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Migid-Hamzza, Jeffery A. "Fat Metabolism in Smooth Dogfish." University of Akron / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=akron1132414091.
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Lam, Shi. "The significance of hepatic stellate cell activation in small-for-size fatty liver graft injury /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B3829686X.
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Grundström, Tobias. "Automated Measurements of Liver Fat Using Machine Learning." Thesis, Linköpings universitet, Datorseende, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-151286.
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The purpose of the thesis was to investigate the possibility of using machine learn-ing for automation of liver fat measurements in fat-water magnetic resonancei maging (MRI). The thesis presents methods for texture based liver classificationand Proton Density Fat Fraction (PDFF) regression using multi-layer perceptrons utilizing 2D and 3D textural image features. The first proposed method was a data classification method with the goal to distinguish between suitable andunsuitable regions to measure PDFF in. The second proposed method was a combined classification and regression method where the classification distinguishes between liver and non-liver tissue. The goal of the regression model was to predict the difference d = pdff mean − pdff ROI between the manual ground truth mean and the fat fraction of the active Region of Interest (ROI).Tests were performed on varying sizes of Image Feature Regions (froi) and combinations of image features on both of the proposed methods. The tests showed that 3D measurements using image features from discrete wavelet transforms produced measurements similar to the manual fat measurements. The first method resulted in lower relative errors while the second method had a higher method agreement compared to manual measurements.
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Banerjee, Rajarshi. "The effects of excess body weight on the heart and liver." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:652e90cd-1f11-4fb6-8a4b-4ce649f72ee5.
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Obesity in adults and children is associated with increased cardiovascular mortality and morbidity. This is forecast to increase markedly in the next decade as childhood obesity is a burgeoning epidemic. Excess weight is clearly associated with insulin resistance, increased circulating triglycerides, and hypertension, all of these are related to progressive heart and liver disease. Ectopic fat deposition within organs is reported to cause lipotoxicity, which may lead to dysfunction and disease, but there have been few human studies to confirm this. This doctoral thesis set out to study the early pathophysiology of obesity in adults and children using in vivo magnetic resonance (MR) imaging and spectroscopy to assess the composition and function of the heart and liver in lean and obese individuals. The central tenet of this project was to establish and validate a clinically viable method for measuring the fat content of viscera safely and accurately, and to determine a normal range for the triglyceride content of the heart and liver. The initial study demonstrated that the heart remodels in response to weight loss, with over 20% reduction in LV mass, confirming that excess weight is genuinely a modifiable risk factor. Then, using spectroscopy, it was established that the healthy myocardium has a median triglyceride content of 0.37% (IQR 0.24% - 0.47%), which increases linearly in overweight and obese adults. Obesity, in the absence of any confounders, was also associated with a 10% reduction in cardiac contractile function. In comparison, healthy liver median lipid content was 0.67% (IQR 0.44% – 0.88%), which increased in obese adults to 2.9% (IQR 1.6% - 7.6%). There was a graded association between ectopic fat deposition in the liver and dyslipidaemia in adults, characterised by increased circulating triglycerides and reduced high-density lipoprotein. This dyslipidaemia may impair reverse cholesterol transport, and thus could be expected to exacerbate weight gain. Among obese and overweight subjects, there were some with severe steatosis and evidence of coexistent hepatic inflammation and fibrosis. To verify the accuracy of these spectroscopic measures for ectopic fat, a blinded, prospective comparison of non-invasive assessment of unselected liver disease in liver biopsy patients was completed. Liver disease presents with one or more of steatosis, fibrosis and haemosiderosis, all of which are associated with adverse cardiovascular outcomes. Fifty patients were recruited, and interobserver variability among pathologists was measured for histological reference standards for fat, fibrosis and iron deposition. MR measures of each of these metrics predicted the fibrosis, steatosis and haemosiderosis scores accurately. This enabled precise tissue characterisation of all forms of liver disease, including steatohepatitis, with one non-invasive test, to allow the diagnosis and monitoring of hepatic conditions. Lastly, all these new biomarkers of early cardiac and liver disease associated with excess weight were applied to obese and lean children, to understand whether ectopic fat played a substantial role in early life. Obese children had increased ectopic fat in their hearts and livers, as well as impaired strain, evidence of dyslipidaemia, and in some cases evidence of active steatohepatitis, comparable to adults with severe disease. The thesis therefore demonstrates that in vivo magnetic resonance techniques can be used for accurate measurement of visceral lipid content. Furthermore, there is evidence of significant ectopic fat deposition in both adults and children, with evidence of organ dysfunction, which raises the possibility that cardiovascular magnetic resonance may be of value to risk stratify obese individuals based on organ involvement. Finally, the developed methods may have broader applicability and offer a promising new method for the non-invasive diagnosis of chronic liver disease in other clinical settings.
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Lewandowski, Paul, and mikewood@deakin edu au. "Liver fat metabolism, obesity and diabetes in Psammomys Obesus." Deakin University. School of Health Sciences, 1999. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050825.111432.
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Defects in fat metabolism are central to the aetiology and pathogenesis of obesity and type II diabetes. The liver plays a central role in these disease states via its regulation of glucose and fat metabolism. In addition, accumulation of fat within the liver has been associated with changes in key pathways of carbohydrate and fat metabolism. However a number of questions remain. It is hypothesised that fat accumulation within the liver is a primary defect in the aetiology and pathogenesis of obesity and type II diabetes. Fat accumulating in the liver is the result of changes in the gene expression of key enzymes and proteins involved with fat uptake, fat transport, fat oxidation, fat re-esterification or storage and export of fat from the liver and these changes are regulated by key lipid responsive transcription factors.
To study these questions Psammomys obesus was utilised. This polygenic rodent model of obesity and type II diabetes develops obesity and diabetes in a similar pattern to susceptible human populations. In addition dietary and environmental changes to Psammomys obesus were employed to create different states of energy balance, which allowed the regulation of liver fat gene expression to be examined. These investigations include: 1) Measurement of fat accumulation and fatty acid binding proteins in lean, obese and diabetic Psammomys obesus. 2) Characterisation of hepatic lipid enzymes, transport protein and lipid responsive transcription factor gene expression in lean, obese and diabetic Paammomys obesus. 3) The effect of acute and chronic energy restriction on hepatic lipid metabolism in Psammomys obesus. 4) The effect of sucrose feeding on the development of obesity and type II diabetes in Psammomys obesus. 5) The effect of nicotine treatment in lean and obese Psammomys obesus, 6) The effect of high dose leptin administration on hepatic fat metabolism in Psammomys obesus.
The results of these studies demonstrated that fat accumulation within the liver was not a primary defect in the aetiology and pathogenesis of obesity and type II diabetes. Fat accumulating in the liver was not the result of changes in the gene expression of key enzymes and proteins involved in hepatic fat metabolism. However changes in the
mRNA level of the transcription factors PPAR∝ and SREBP-1C was associated with
the development of diabetes and the gene expression of these two transcription factors was associated with changes in diabetic status.
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Gubík, Ladislav. "Automatic quantification of fat in liver using Computer Vision /." Leeds : University of Leeds, School of Computer Studies, 2008. http://www.comp.leeds.ac.uk/fyproj/reports/0708/Gubik.pdf.
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Crabtree, Christopher David. "Effects of Controlled Hypocaloric Ketogenic and Low-Fat Diets on Liver Fat in Overweight/Obese Adults." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1586780375128754.
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Shoebotham, Karen. "The relationship between liver fat content and unenhanced computed tomography." [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-12092008-161843/.
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Lam, Shi, and 林璽. "The significance of hepatic stellate cell activation in small-for-sizefatty liver graft injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45012933.
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Lee, Sang Jun. "CEACAM1 : a common regulator of fat metabolism and cell proliferation." Connect to full text in OhioLINK ETD Center, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1218146004.
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Dissertation (Ph.D.)--University of Toledo, 2008."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 74-82, 116-124, 146-192.
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Orabi, Danny Ahmad. "The Effects of High Fat Diet on Liver Disease and Hepatocellular Carcinoma." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1619778405639812.
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Evans, Alison. "The splanchnic circulation and chronic heart failure." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324047.
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Pisto, P. (Pauliina). "Fat accumulation in liver and muscle:association with adipokines and risk of cardiovascular events." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526201351.
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Abstract The prevalence of obesity is dramatically on the rise in the Western world. Obesity is associated with several chronic diseases, including diabetes and cardiovascular disease (CVD). Non-alcoholic fatty liver disease occurs when fat is ectopically stored in the liver. It is closely associated with serious metabolic abnormalities. Non-alcoholic fatty liver disease ranges from simple hepatic steatosis with no inflammation to hepatic steatosis with a necroinflammatory component, which may lead to cirrhosis and liver failure. Adiponectin is an adipokine that is solely secreted by adipocytes and has anti-inflammatory, antiatherogenic and insulin-sensitizing properties. Adipose tissue inflammation contributes to reduced plasma adiponectin levels in obesity leading to further metabolic complications. Adiponectin may be a mediator between obesity and fat accumulation in the liver and skeletal muscle. Fatty liver may play a role in the pathogenesis of CVD. Mortality data show that CVD as the cause of death accounts for almost half of all deaths in Finland. Traditional risk factors for CVD are age, gender, smoking, high low-density lipoprotein level, high blood pressure and diabetes. The aim of the thesis was to investigate the mediators of fat accumulation in the liver and skeletal muscle as well as the role of fatty liver in the future risk for CVD. If one considers the peptide hormones, then adiponectin turned out to be the strongest independent indicator of the brightness of the liver. In addition, an association between a low adiponectin concentration and large muscle fiber size was observed, and this was not dependent on the amount of total fatness. Furthermore, severe fatty liver increased the risk for cardiovascular events, predicted the risk for death from all causes and death from CVD in a long follow-up. Insulin sensitivity seemed to play a more dominant role in developing cardiovascular events. In conclusion, this study demonstrates that adiponectin may have an important effect on fat accumulation in the liver and skeletal muscle. Adiponectin could be a target when considering the treatment and prevention of ectopic fat accumulation. Fatty liver seems to play a significant role in developing cardiovascular event and mortality to CVDTiivistelmä Lihavuus on kasvava ongelma länsimaissa. Lihavuudella on todettu olevan yhteyttä lukuisiin kroonisiin sairauksiin, kuten diabetekseen ja sydän- ja verisuonitautiin. Ei-alkoholiperäinen rasvamaksa aiheutuu rasvan kertymisestä maksaan. Tilan on todettu liittyvän läheisesti vaikeisiin aineenvaihdunnan häiriöihin. Ei-alkoholiperäinen rasvamaksa vaihtelee vakavuusasteeltaan poikkeavasta rasvan kertymisestä tulehdukseen, joka voi edelleen johtaa kirroosiin ja maksan toiminnan pettämiseen. Adiponektiini on pääasiassa rasvakudoksen erittämä hormoni, jolla on tulehdusta hillitseviä, ateroskleroosilta suojaavia ja insuliinia herkistäviä ominaisuuksia. Rasvakudoksen tulehdustila myötävaikuttaa alentuneeseen adiponektiinipitoisuuteen, joka voi johtaa vaikeutuneisiin aineenvaihdunnan häiriöihin. Adiponektiinin epäillään olevan välittäjäaine lihavuuden ja rasvamaksan ja lihaksensisäisen rasvan välillä. Rasvamaksan ja kardiovaskulaarisairauksien välillä saattaa olla yhteys. Sydän- ja verisuonisairaudet aiheuttavat lähes puolet kuolemista Suomessa. Perinteisiä kardiovaskulaaritaudin riskitekijöitä ovat ikä, sukupuoli, tupakointi, korkea LDL-kolesteroli, korkea verenpaine ja diabetes. Tutkimuksemme tavoitteena oli selvittää maksan ja lihaksen rasvan kertymiseen myötävaikuttavia tekijöitä sekä rasvamaksan vaikutusta riskiin sairastua sydän- ja verisuonisairauksiin. Tutkimuksessa havaittiin, että lihavuuteen liittyvistä hormoneista adiponektiini oli vahvin itsenäinen myötävaikuttaja rasvamaksan kehittymisessä. Plasman alentunut adiponektiinipitoisuus yhdistyi kasvaneeseen lihassolun kokoon riippumatta henkilöiden rasvakudoksen määrästä. Seurantatutkimuksen mukaan vaikeasti rasvoittunut maksa lisäsi riskiä sairastua kardiovaskulaaritautiin, ennusti yleistä kuolemanriskiä ja kuolemaa kardiovaskulaaritautiin. Insuliiniherkkyydellä näytti olevan merkittävä rooli sydän- ja verisuonitautitapahtumissa. Tutkimus osoittaa, että adiponektiinillä saattaa olla keskeinen rooli rasvan kertymisessä maksaan ja lihakseen. Adiponektiini voi olla keskeinen tutkimuskohde kehiteltäessä hoitomuotoja ja ehkäisymenetelmiä rasvakudoksen ulkopuolisen rasvan kertymiseen. Rasvamaksan rooli sairaalahoitoon tai kuolemaan johtavissa ateroskleroottisissa tapahtumissa on ilmeinen
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Liang, Wentao. "Myostatin promotes liver fat accumulation through activation of the mTOR-SREBP-1c pathway." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12479.
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Thesis (M.A.)--Boston UniversityMyostatin is a cytokine primarily expressed in skeletal muscle and heart muscle and acts as a negative regulator for muscle development. Inhibition of myostatin by genetic and pharmacological approaches improves metabolic health, which has been generally considered as secondary to the hypermuscularity and insulin hyper-sensitivity. Although the receptor for myostatin is ubiquitously expressed, whether and how myostatin interacts with other metabolically important cell types remain largely unknown. In this work, we provide multiple lines of evidence that myostatin directly interacts with hepatocytes. Furthermore, we show for the first time that myostatin enhances insulin signaling in both cultured hepatocytes and in mouse liver. Mice injected with adena-associated virus encoding myostatin propeptide, an endogenous myostatin inhibitor, were partially protected from diet-induced liver fat accumulation and reduced lipogenic gene expression. Consistent with the in vivo findings, increased lipid accumulation was found in cells treated with myostatin peptide or transfected with myostatin construct. Myostatin promotes the lipogenic effect of insulin by enhancing nuclear translocation of SREBP-1c, the master lipogenic transcription factor and increases expression of its downstream target genes. This effect was found to be associated with myostatin-related mTOR activation. Blocking mTOR activation by rapamycin prevents myostatinassociated increase of nuclear SREBP-1 c and its downstream lipogenic enzymes. In summary, this work identified liver as a direct target of myostatin, providing the first evidence that myostatin has opposite impacts on insulin signaling in muscle cells and hepatocytes. Our data also provided a novel mechanism for the long-term metabolic protection afforded by anti-myostatin treatments demonstrated in this work as well as elsewhere.
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Abrahams, Celeste H. "The modulation of effect of fatty acids on the lipid in colon epithelial mucosa in Vivo /." Online access, 2009. http://etd.uwc.ac.za/usrfiles/modules/etd/docs/etd_gen8Srv25Nme4_3963_1275516655.pdf.
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Iggman, David. "Dietary Fatty Acids and Cardiometabolic Risk : Influence on Lipoproteins, Insulin Resistance and Liver Fat." Doctoral thesis, Uppsala universitet, Klinisk nutrition och metabolism, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-252066.
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The aim of this thesis was to investigate how dietary fatty acids affect the risk for cardiometabolic disease, i.e. cardiovascular disease (CVD), type 2 diabetes and obesity. The overall hypothesis was that unsaturated fatty acids and especially the predominant polyunsaturated fatty acid (PUFA) linoleic acid (LA), 18:2n-6, would decrease cardiometabolic risk compared with saturated fatty acids (SFAs), in line with current recommendations to partly replace dietary SFA with PUFA. Papers I and V were observational studies based on the community-based cohort Uppsala Longitudinal Study of Adult Men (ULSAM). Adipose tissue fatty acid composition was determined as biomarker for dietary fat intake. Studies II, III and IV were randomised short-term interventions on human volunteers, in which different dietary fats were provided to the participants. In 71-year-old men, adipose tissue LA and α-linolenic acid (18:3n-3) were associated with insulin sensitivity (euglycaemic clamp), although this association was diminished for LA after adjusting for lifestyle variables. Different SFA displayed divergent associations; only palmitic acid (16:0) was inversely associated with insulin sensitivity (Paper I). In Cox regression analyses, LA was modestly associated with decreased all-cause mortality, but not CVD mortality during 15 years follow-up (Paper V). In a 3+3-week cross-over study on 20 weight-stable volunteers with dyslipidaemia, all foods were provided. A rapeseed oil-based diet distinctly lowered low-density lipoprotein cholesterol and triglycerides compared with a dairy-fat based diet (butter, cream and fatty cheese). Insulin sensitivity or coagulation factors were not affected (Paper II). In a 10-week randomised trial on 67 abdominally obese participants, PUFA (mostly sunflower oil) decreased liver fat compared with SFA (mostly butter) under isocaloric conditions. In individuals considered highly compliant to study diets, lipoproteins were also decreased during the PUFA diet (Paper III). In a 7-week double-blind randomised trial on 41 healthy volunteers, PUFA (sunflower oil) decreased the total:HDL cholesterol ratio compared with SFA (palm oil) during moderate weight gain (1.5 kg) (Paper IV). In conclusion, LA (PUFA) intake is associated with decreased cardiometabolic risk compared with higher SFA intake, overall supporting a beneficial role of non-tropical vegetable oils in place of solid fats in preventing fatty liver and cardiometabolic disorders.
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Thoma, Christian. "Exercise, glucose control and liver fat : providing the evidence for translation into clinical care." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2340.
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Non-alcoholic fatty liver disease (NAFLD) has become the most common form of liver disease throughout much of the World. It affects between one in five and one in three adults in the general population. It is now believed to be the leading cause of liver cirrhosis and hepatocellular carcinoma. However, the majority of people with NAFLD do not go on to develop terminal liver disease but instead have an uncertain prognosis that can often include type 2 diabetes, cardiovascular disease, and/or non-hepatic cancers. Indeed, NAFLD is frequently accompanied impaired glucose control, and almost always suboptimal insulin sensitivity. This thesis explores the only currently recommended therapy – weight reduction by lifestyle modification. It reviews the published evidence supporting this recommendation by applying a systematic approach to review the literature, but examines the findings in the broader context of common NAFLD comorbidities and sequelae. It also examines interaction of age and physical activity with liver fat, specifically in women, using both primary and secondary research methods. Finally, it explores exercise, particularly high-intensity intermittent training as a means to reduce liver fat, improve body composition, and attenuate insulin resistance independent of weight change and dietary advice. The principle finding is that, although the literature supports the recommendation of weight reduction, exercise can be an effective therapy to reduce liver fat and improve glucose control/insulin independent of weight change in adults with NAFLD. High-intensity intermittent training is particularly ii effective for liver fat reduction, improves glucose control/insulin resistance, and results in positive changes to body composition.
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Cain, James. "Characterizing the role of dietary fat in the development and progression of liver dysfunction." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/903.
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Obesity and metabolic dysfunction are worldwide health epidemics and they have grown to unprecedented levels. Human NAFLD is directly linked to obesity and metabolic dysfunction, so attention was given to elucidating a more complete understanding of the liver's role in mediating the metabolically healthy obese phenotype and to better characterizing the potential contribution of dietary fat and fatty acids as a therapeutic supplement to obesogenic diets. Specifically, flaxseed is high in α-linolenic acid (ALA; 18:3 n-3) and low in linoleic acid (LA; 18:2 n-6), and contains multiple other components such as fiber and lignans, and was investigated for its high potential to modify obesity phenotype and fatty liver disease. Additionally, we explored the temporal effect of initiating high-fat diets in various phases of adulthood. However, work in this field is complicated by an ongoing search for appropriate preclinical animal models of NAFLD as they have not been able to replicate the full spectrum of human NAFLD. As such, this dissertation sought to explore fatty liver disease in popular murine models of overnutrition, as well as a novel hen model. Major findings from this work showed that (1) exposure to a high-fat diet during early adulthood preserves metabolic homeostasis, modifies liver morphology, and protects against obesity-related disease, (2) dietary enrichment with flaxseed is capable of increasing tissue n3PUFA content, but this appeared to be only weakly related to metabolic and histological outcomes, and (3) there are limitations to the laying hen as a model of NAFLD as the pathogenic changes may not adequately match the human condition.
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Yang, Yan. "CEACAM1 : a molecular link between fat metabolism and insulin clearance." Connect to full-text via OhioLINK ETD Center, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1115060085.
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Thesis (Ph.D.)--Medical College of Ohio, 2004.In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences. Major advisor: Sonia Najjar. Includes abstract. Document formatted into pages: v, 167 p. Bibliography: pages 117-165.
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Toyama, Yoshiro. "Impact of Obstructive Sleep Apnea on Liver Fat Accumulation According to Sex and Visceral Obesity." Kyoto University, 2015. http://hdl.handle.net/2433/202801.
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Owen, Carl. "The role of adipocyte and liver protein tyrosine phosphatase 1B (PTP1B) in glucose homeostasis and insulin sensitivity." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=203411.
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Kohan, Alison Bloom. "Mechanism by which dietary polyunsaturated fat regulates lipogenic gene expression." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10605.
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Thesis (Ph. D.)--West Virginia University, 2009.Title from document title page. Document formatted into pages; contains viii, 141 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Wu, Nan. "Regulation of hepatic inflammatory response and lipid metabolism in metabolic disease." The American Physiological Society, 2009. http://hdl.handle.net/1993/23352.
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Hyperhomocysteinemia, an elevation of blood homocysteine levels, is a metabolic disorder associated with dysfunction of multiple organs. Previous studies have shown that hyperhomocysteinemia is related to fatty liver. However, the underlying mechanism remains speculative. The objective of the present study is to investigate the regulatory mechanism of hepatic inflammatory response and cholesterol metabolism during metabolic disorders.
In the present study, hyperhomocysteinemia was induced in Sprague-Dawley rats by feeding a high-methionine diet. The mRNA and protein expression of cyclooxygenase-2 (COX-2), a pro-inflammatory factor, were significantly elevated in the liver of hyperhomocysteinemic rats. An activation of NF-B and a stimulation of oxidative stress were observed in the same liver tissue in which COX-2 was induced. Inhibition of NF-B or oxidative stress effectively abolished hepatic COX-2 expression, inhibited the formation of inflammatory foci, and improved liver function.
Activity of HMG-CoA reductase, the rate-limiting enzyme of cholesterol biosynthesis, was markedly elevated in the liver of hyperhomocysteinemic rats, which may contribute to the hepatic lipid accumulation induced by hyperhomocysteinemia. Administration of Berberine (5mg/ kg body weight/ day for 5 days) inhibited HMG-CoA reductase activity via upregulating AMP-activated protein kinase (AMPK)-mediated phosphorylation of HMG-CoA reductase. Berberine treatment reduced hepatic cholesterol content and ameliorated liver function.
In addition, the regulatory mechanism of HMG-CoA reductase activation was investigated in C57BL/6 mice fed a high-fat diet. There was a significant increase in hepatic HMG-CoA reductase mRNA and protein expression as well as enzyme activity. The DNA binding activity of sterol regulatory element binding protein (SREBP)-2 (a transcription factor of HMG-CoA reductase) and Sp1 (a transcription factor of SREBP-2) were both increased in the liver of mice fed a high-fat diet. The in vitro study in palmitic acid-treated HepG2 cells further confirmed that inhibition of Sp1 by siRNA transfection abolished palmitic acid-induced SREBP-2 and HMG-CoA reductase mRNA expression.
In conclusion, the present study have demonstrated that (1) Hepatic COX-2 expression is induced via oxidative stress mediated NF-B activation during hyperhomocysteinemia; (2) Dietary berberine reduces cholesterol biosynthesis by elevating AMPK-mediated HMG-CoA reductase phosphorylation; (3) HMG-CoA reductase is upregulated by Sp1-mediated SREBP-2 activation in the liver during high-fat diet feeding.
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Rosqvist, Fredrik. "Dietary Fatty Acids, Body Composition and Ectopic Fat : Results from Overfeeding Studies in Humans." Doctoral thesis, Uppsala universitet, Klinisk nutrition och metabolism, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-280949.
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The aim of this thesis was to investigate the effects of dietary fatty acids on body composition and ectopic fat in humans, with emphasis on the role of the omega-6 polyunsaturated fatty acid (PUFA) linoleic acid (18:2n-6) and the saturated fatty acid (SFA) palmitic acid (16:0). The overall hypothesis was that linoleic acid would be beneficial compared with palmitic acid during overfeeding, as previously indicated in animals. Papers I, II and IV were double-blinded, randomized interventions in which different dietary fats were provided to participants and Paper III was a cross-sectional study in a community-based cohort (PIVUS) in which serum fatty acid composition was assessed as a biomarker of dietary fat intake. In Paper I, overfeeding with sunflower oil (n-6 PUFA) for 7 weeks caused less accumulation of liver fat, visceral fat and total body fat (as assessed by MRI) compared with palm oil (SFA) in young and lean subjects despite similar weight gain among groups. Instead, sunflower oil caused a larger accumulation of lean tissue. In Paper II, plasma from Paper I was analyzed with NMR-based metabolomics, aiming to identify metabolites differentially affected by the two dietary treatments. Acetate decreased by PUFA and increased by SFA whereas lactate increased by PUFA and decreased by SFA. In Paper III, the proportion of linoleic acid in serum was inversely associated with contents of visceral-, subcutaneous- and total body adipose tissue whereas the proportion of palmitic acid was directly associated with visceral- and total body adipose tissue in 70-year old men and women. In Paper IV, overfeeding with sunflower oil for 8 weeks caused less accumulation of liver fat compared with palm oil also in overweight and obese subjects. SFA increased visceral fat in men only. Accumulation of lean tissue was similar between groups. In conclusion, SFA (palmitic acid) from palm oil promotes marked liver fat accumulation in both normal-weight and overweight/obese subjects during overeating, whereas n-6 PUFA (linoleic acid) from sunflower oil prevents such liver fat accumulation. Diverging effects of SFA and PUFA on visceral adipose tissue and lean tissue may only be applicable in some groups and/or circumstances. These results imply that negative effects associated with weight gain (e.g. fatty liver) may be partly counteracted by the type fat in the diet, overall supporting a beneficial role of diets higher in unsaturated fat compared with saturated fat for preventing liver fat accumulation.
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Zhang, Linda S. "Apolipoprotein A-V: A Novel Liver-gut Signal Protein that Regulates the Production of Chylomicrons." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1439305376.
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Al-Share, Qusai Y. "Reduction of hepatic CEACAM1 levels : an early mechanism of insulin resistance induced by high-fat diet." Connect to full text in OhioLINK ETD Center, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1201787222.
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Dissertation (Ph.D.)--University of Toledo, 2007."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 120-176.
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Penke, Melanie, Per S. Larsen, Susanne Schuster, Morten Dall, Benjamin A. H. Jensen, Theresa Gorski, Andrej Meusel, et al. "Hepatic NAD salvage pathway is enhanced in mice on a high-fat diet." Elsevier, 2015. https://ul.qucosa.de/id/qucosa%3A38585.
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Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme for NAD salvage and the abundance of Nampt has been shown to be altered in non-alcoholic fatty liver disease. It is, however, unknown how hepatic Nampt is regulated in response to accumulation of lipids in the liver of mice fed a high-fat diet (HFD). HFD mice gained more weight, stored more hepatic lipids and had an impaired glucose tolerance compared with control mice. NAD levels as well as Nampt mRNA expression, protein abundance and activity were significantly increased in HFD mice. Enhanced NAD levels were associated with deacetylation of p53 and Nfκb indicating increased activation of Sirt1. Despite impaired glucose tolerance and increased hepatic lipid levels in HFD mice, NAD metabolism was significantly enhanced. Thus, improved NAD metabolism may be a compensatory mechanism to protect against negative impact of hepatic lipid accumulation.
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Abel, Stefan. "Fatty acids as cancer preventive tools in the dietary modulation of altered lipid profiles associated with hepatocarcinogenesis." Thesis, University of the Western Cape, 2005. http://etd.uwc.ac.za/index.php?module=etd&.
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This thesis consists of a brief description on cancer, carcinogenesis, the changes in the type and level of dietary fat available in our diets over time and association with the development of certain diseases. The main focus of this research was on omega 6 and omega 3 essential fatty acids (EFA) and their interaction with regards to carcinogenesis.
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Neves, Christian André Fernandes. "Methylglyoxal-induced glycation changes liver lipid content in high-fat diet-fed rats, causing glucose and lipid systemic dysmetabolism." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/14597.
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Mestrado em Biomedicina MolecularFatty liver disease is simultaneously a cause and a consequence of type 2 diabetes. Hepatic lipid metabolism is altered in obese patients, causing insulin resistance. More, inhibition of insulin signaling may also affect hepatic lipid metabolism, causing a feedback that may lead to hepatic steatosis, common in such patients. In this work, we intended to assess the role of glycation (methylglyoxal-induced) in the hepatic lipid metabolism of high-fat diet-fed rats, using lipidomic approaches and magnetic resonance imaging, which identify hepatic lipid species, including phospholipids (PL), triglycerids (TG), diacylglycerols (DAG) and fatty acids (FA). Wistar rats were maintained during 4 months with methylglyoxal (MG) supplementation (100mg/Kg/day) (MG group), a high-fat diet rich in TG (HFD group) or both (HFDMG group) and compared with controls feeding a standard diet (n=6/ group). Lipidomic approaches, namely liquid chromatography - mass spectrometry (LC-MS) and gas chromatography (GC) were used to determine liver composition in PL, TG and FA. Non-invasive 1H nuclear magnetic resonance (NMR) spectroscopy (9 Tesla) of liver tissues in vivo was used to determine lipid species, such as TG and DAG. The total and phosphorylated levels of the mediators of the insulin receptor pathway and lipid oxidation were determined by western blotting. High-fat diet-fed (HFD) rats showed increased body weight in relation to controls, but this effect was partially inhibited by MG supplementation (HFDMG group). Moreover, HFDMG group showed increased plasma free fatty acid levels, hyperinsulinemia, insulin resistance and glucose intolerance. In liver, lipidomic techniques and 1H NMR showed increased fat mass in the liver of HFD and HFDMG rats. HFD rats, but not HFDMG, showed increased total levels of the 18:1 fatty acid (common in high-fat diets). Despite no differences were observed for HFD group, HFDMG rats showed decreased fraction of unsaturated lipids and increased fraction of saturated lipids. This difference was obtained due to a decrease in monounsaturated FA. Regarding lipid esterification, HFDMG group showed lower percentage of esterified glycerol carbons, suggesting an increased concentration of DAG in relation to TG. In accordance, this group showed higher fatty acids/glycerol ratio, suggesting increased liver non-esterified fatty acid levels. Western Blotting analyses showed decreased activation of insulin pathway, especially HFDMG group, as well as decreased activation of the insulin receptor in HFDMG group. Data suggest that glycation changes lipid metabolism in a context of hyperlipidemia, possibly contributing to hepatic lipotoxicity and to accelerate progression of insulin resistance and fatty liver disease.
O fígado gordo é simultaneamente uma causa e consequência da diabetes mellitus tipo 2. O metabolismo lipidico-hepático (MLH) encontra-se alterado em obesos, causando insulino-resistência. A diminuição da sinalização da via da insulina pode igualmente afetar o MLH, estimulando o desenvolvimento de esteatose hepática, comum nos doentes. Neste trabalho, pretende-se analisar o papel da glicação (induzida por metilglioxal) no MLH em ratos com dieta gorda, através de técnicas de lipidómica e ressonância magnética, para identificar as espécies lipídicas hepáticas, tais como fosfolípidos (FL), triglicéridos (TG), diacilgliceróis (DAG) e ácidos gordos (AG). O modelo animal usado foi o rato Wistar, mantido nos últimos 4 meses, antes de completar 1 ano de idade, com metilglioxal (100mg/Kg/dia) (grupo MG), com dieta gorda rica em TG (grupo HFD) ou com ambas (grupo HFDMG) e comparados com os controlos com dieta normal (n=12/grupo). As técnicas de lipidómica usadas foram cromatografia líquida com espetrometria de massa e cromatografia gasosa para determinar a composição hepática de PL, TG e AG. Usou-se também espectroscopia (9 Tesla), não invasiva, de ressonância magnética nuclear 1H (NMR) nos ratos vivos para determinar os TG e DAG hepáticos. Os mediadores proteicos totais e fosforilados da via da insulina e da oxidação lipídica no fígado também foram analisados por western blot. Os ratos, com dieta gorda (HFD), aumentaram o peso corporal, mas o efeito foi parcialmente inibido pelo metilglioxal (HFDMG). Além disso, o grupo HFDMG apresenta um aumento dos ácidos gordos livres no plasma, hiperinsulinemia, insulino-resistência e intolerância à glicose. No fígado, as técnicas de lipidómica e NMR mostraram um aumento da massa gorda no fígado nos grupos HFD e HFDMG, mas apenas no grupo HFD se verifica o aumento do AG 18:1 (comum na dieta). Apesar de não haver diferença significativa no grupo HFD, o grupo HFDMG apresenta uma diminuição dos AG insaturados e aumento dos saturados; isto deve-se à diminuição dos monoinsaturados neste grupo. Quanto à esterificação dos glicerolípidos, o grupo HFDMG apresenta uma menor percentagem da total esterificação dos gliceróis, sugerindo o aumento dos DAG, em relação aos TG. Também, este grupo apresenta um ratio AG/glicerol aumentado, ou seja, com aumento de AG não esterificados. A análise por western blot mostrou uma diminuição da via do receptor da insulina especialmente no grupo HFDMG. Em suma, estes resultados sugerem que a glicação causa alterações do metabolismo lipidico-hepático num contexto de hiperlipidemia, contribuindo possivelmente para a lipotoxicidade hepática, progressão acelerada de insulino-resistência e patologia do fígado gordo.
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Saffaf, Jasem. "Klinische Bedeutung der Leberverfettung bei Kühen." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-170356.
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Problem: Die Leberverfettung wird als eine der wichtigsten metabolischen Störungen in der Frühlaktation bei Milchkühen und als Grund für Gesundheits- einschließlich Reproduktionsstörungen angesehen. Zielstellung: Deshalb wurden in dieser Studie folgende Fragestellungen bearbeitet: a) Bedeutung der klinischen und labordiagnostischen Befunde bei der Erstuntersuchung kranker Kühe, insbesondere des Leberfettes, b) Beziehungen zwischen dem Leberfettgehalt und verschiedenen Laborparametern, c) Beziehungen zwischen dem Leberfettgehalt, den Krankheiten und dem Behandlungserfolg, d) prognostische Bedeutung des Leberfettgehaltes sowie klinisch-chemischer und hämatologischer Blutparameter. Material und Methoden: Dazu wurden chronologisch 312 in die MTK Leipzig eingelieferte Rinderpatienten entsprechend klinisch und labordiagnostisch einschließlich Leberbiopsie untersucht und die Befunde der Erstuntersuchung ausgewertet. Ergebnisse: Bei 312 Rinderpatienten wurden in 18 Krankheitsgruppen, z.T. nach Verlauf und Schweregraden untersetzt, 196 links- und 40 rechtseitige Labmagenverlagerungen (LMV), 11 Labmagen- (LM) Ulcera, 182 Ketosen, 96 Mastitiden, 178 Endometritiden, 7 Retentio. sec., 7 puerperale Septikämien und 6 Multiorganversagen, 42 Indigestion, 31 Enteritis, 46 Peritonitiden, 30 Festlieger und 18 Pneumonien diagnostiziert. Die Kühe verteilten sich auf vier Leberfettklassen wie folgt: ≤6% =14,7%; 6 bis ≤15% = 37,5%; 15 bis ≤30% = 31,1% sowie >30% = 16,7%. Die Heilungsrate betrug in den ersten drei Leberfettklassen 80,4%, 83,8% bzw. 86,6%. Ein Zusammenhang zwischen der Heilungsrate und dem Leberfettgehalt war bis zu ≤30% nicht erkennbar. In der Leberfettklasse >30% sank die Heilungsrate auf 61,5%; bei >40% verschlechterte sie sich unter 50%. Dem entsprach das Verhalten verschiedener Laborparameter. Erst bei einem Leberfettgehalt >30%, besonders bei >45%, wurden, z.T. unabhängig vom Krankheitsausgang, die BHB-, Bilirubin- und Glucose-Konzentrationen sowie AST-, CK-, LDH-, GGT- und GLDH-Aktivitäten signifikant höher bzw. die anorg. Phosphat- (Pi) und Cholesterol-Konzentrationen niedriger. Mit dem Leberfettgehalt korrelierten am engsten (p<0,001) die Parameter BHB (0,620) und FFS (0,615), LDH (0,579), Bilirubin (0,367), AST (0,359), Cholesterol (-0,278), Laktat (-0,253), Hämoglobin (0,214), CK (0,207), Leukozyten (-0,202) sowie innere Körpertemperatur (0,210). Die Bedeutung dieser Beziehungen ist relativ. Sowohl Sensitivität und Spezifität waren für Pi (<1,25 mmol/l) >0,7, für Cholesterol (< 1,5 mmol/l) und Albumin (<30 g/l) >0,6 sowie für BHB, Harnstoff und Gesamteiweiß >0,5. Eine hohe Spezifität >0,8 bei geringer Sensitivität hatten K (<3,0 mmol/l) und segmentkernige neutrophile Granulozyten (< 4,6 G/l), eine hohe Sensitivität >0,8, aber geringe Spezifität Bilirubin (>5,3 μmol/l), AST (>80 U/l) sowie CK (>200 U/l). Hinsichtlich Krankheitsausgang und damit der prognostischen Nutzbarkeit waren die Flächen (AUC) unter den ROC-Kurven nur für K (0,37), Bilirubin (0,62), AST (0,61) und für Leberfett (0,60) schwach gesichert. Die leberspezifischen Enzyme GGT und GLDH korrelierten nur schwach mit 0,126 (p<0,05) sowie 0,192 (p<0,001) mit dem Leberfett. Das stellt ihre diagnostische Bedeutung nicht in Frage, sondern verdeutlicht, dass bei den analysierten Krankheiten keine stärkeren Leberschäden auftraten. Die bei den Korrelations-, Sensitivitäts- und Spezifitätsberechnungen sowie z.T. ROC-/AUC-Analysen informativen Parameter LDH, AST, CK, K, Pi, Bilirubin (>20 μmol/l) und Leukozyten weisen auf entzündliche Prozesse hin. Die in allen Leberfettklassen erhöhten Glucose-Konzentrationen, bes. bei >30% Leberfett und Ex. letalis, ordnen sich damit zumindest teilweise als Folge einer Insulinresistenz ein. Kühe mit LMV hatten i.d.R. zusätzliche Störungen: zu 58% Ketosen, 57% Endometritiden, 6,4% Retentio sec., puerperale Septikämie und Multiorganversagen, 30,8% Mastitiden, 14,7% Peritonitiden, 9,9% Enteritiden, 9,6% Festliegen, 5,8% Pneumonien sowie 3,5% Labmagenulcera. Außerdem kamen zu 13,5% Indigestionen vor. Die Heilungsrate lag bei links- und rechtseitigen LMV, Mastitiden, Endometritiden und Enteritiden zwischen 89% bis 70% und bei Indigestionen sowie akuten Peritonitiden zwischen 70 und 60%. Bei chronischen Peritonitiden, Pneumonien, Retentio sec., puerperalen Septikämien, Festliegen, LM-Ulcera und Multiorganversagen sank sie von 50% bis auf 0%. Der Leberfettgehalt schwankte bei LMV, Mastitiden, Endometritiden, chronischen Peritonitiden und Indigestionen zwischen 6% und 19%. Er stieg mit schlechterem Therapieergebnis bei Retentio sec., Pneumonien, akuten Peritonitiden puerperalen Septikämien, LM-Ulcera und Enteritiden bis gegen 30% und betrug bei Festliegern, hochgradigen Endometritiden sowie Multiorganversagen bis gegen 40%. Schlussfolgerungen: Leberfett bis ≤30% ist klinisch unbedeutend. Der Trend zu höherem Leberfett und schlechterer Heilungsrate unterstreicht die Bedeutung stark entzündlicher Grundkrankheiten für die Krankheitsentwicklung und den Therapieerfolg. Die Leberschwimmprobe kann für die Anwendung in der Praxis empfohlen werdenProblem: The fatty liver is considered to be one of the most important metabolic disorders in early lactation in dairy cows and is a reason for poor health, including reproductive disorders. Objective: Therefore the following questions in this study were studied: a) importance of the clinical and laboratory findings at the initial examination of sick cows, especially the liver fat, b) relationships between liver fat content and various laboratory parameters, c) the relationship between the liver fat content, diseases and the treatment success, d) prognostic significance of liver fat content and clinical-chemical and hematological blood parameters. Material and Methods: For 312 bovine patients, provided chronological to the MTK Leipzig, were examined according to clinical and laboratory investigations including liver biopsy and evaluated the findings of the initial examination. Results: In 312 cattle, divided in 18 disease groups, 196 left and 40 right-sided abomasal displacements (LMV), 11 abomasal ulcers, 182 ketoses, 96 mastitis, endometritis 178, 7 Retentio sec., puerperal sepsis, 7 and 6 multi organ failure, 42 Indigestion, 31 enteritis, 46 peritonitis, 30 downer cows and 18 pneumonia diagnosed. The cows were grouped in four liver fat classes as follows: ≤6% = 14.7%; 6 to ≤15% = 37.5%; 15 to ≤30% = 31.1% and> 30% = 16.7%. The cure rate was in the first three classes of liver fat 80.4%, 83.8% and 86.6% respectively. A relationship between the cure rate and the liver fat content was not recognizable to ≤30%. In the liver fat class> 30% cure rate dropped to 61.5%; at> 40% it worsened <50%. This corresponded to the behavior of various laboratory parameters. Only when liver fat content> 30%, particularly at> 45%, were partly regardless of the outcome of the disease, the BHB, bilirubin and glucose concentrations as well as AST, CK, LDH, GGT and GLDH activities were significantly higher and the inorg. Phosphate (Pi) and cholesterol concentrations low. The liver fat content correlated most closely (p <0.001), the parameters BHB (0.620) and FFS (0.615), LDH (0.579), bilirubin (0.367), AST (0.359), cholesterol (-0.278), lactate (-0.253), hemoglobin (0.214), CK (0.207), leukocytes (-0.202) and internal body temperature (0.210). The significance of these relationships is relative. Sensitivity and specificity were Pi (<1.25 mmol / l)> 0.7, to cholesterol (<1.5 mmol / l) and albumin (<30 g / l)> 0.6, and for BHB, urea, and total protein> 0.5. High specificity> 0.8 for low sensitivity had K (<3.0 mmol / l) and segment neutrophilic granulocytes (<4.6 g / l), a high sensitivity> 0.8, but low specificity bilirubin (> 5 , 3 mol / l) AST (> 80 U / l) and CK (> 200 U / l). With regard to disease outcome and thus the prognostic value of the area under the curve (AUC) for K (0.37), bilirubin (0.62), AST (0.61) and liver fat (0.60) were weakly secured. The liver-specific enzymes GGT and GLDH correlated only weakly with 0.126 (p <0.05) and 0.192 (p <0.001) with the liver fat. This do not challenges their diagnostic significance, but it makes clear that in the studied diseases no greater liver damage occurred. Whereas the correlation, sensitivity and specificity calculations as well as some ROC/AUC analysis informative parameter LDH, AST, CK, C, Pi, bilirubin (> 20 μmol/l) and leukocytes indicate inflammatory processes. The increased liver fat in every group glucose concentrations, esp. at liver fat > 30% and ex. letalis, thus organize at least partially as a result of insulin resistance. Cows with DA had usually. additional disorders: 58% ketoses, 57% endometritis, 6.4% Retention sec, puerperal septicemia and multi-organ failure, 30.8% mastitis, 14.7% of peritonitis, enteritis 9.9%, 9.6% recumbency, 5.8% pneumonia and 3.5% ulceration of the abomasum. Furthermore, came to 13.5% before indigestion. The cure rate of left and right DA, mastitis, endometritis and enteritis were between 89% to 70% and for indigestion and acute peritonitis 70-60%. In chronic peritonitis, pneumonia, Retention sec., Puerperal septicemia, recumbency, abomasum ulcers and multiple organ failure they fell from 50% to 0%. The liver fat content varied with DA, mastitis, endometritis, chronic peritonitis and indigestion between 6% and 19%. He rose with a worse clinical outcome in Retentio sec., Pneumonia, acute peritonitis puerperal septicemia, DA ulcers and enteritis up to 30% and was at Festliegern, high-grade endometritis and multiorgan failure until about 40%. Conclusions: Liver fat to ≤30% is clinically insignificant. The trend towards higher liver fat and poorer cure rate underscores the importance of strong inflammatory diseases reason for the disease development and therapeutic success. The copper sulphate test according to Herdt can be recommended for use in practice
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Baker, Callum John. "Effects of Exercise Training on Liver Fat and Circulating Immune Markers in People who are Obese or Overweight with Normal or Dysglycaemia." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/29173.
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Aims: This thesis aimed to examine the efficacy of exercise to reduce liver fat firstly via meta-analysis and then through investigation of a novel exercise modality; low volume high intensity interval training with combined progressive resistance training. This thesis also investigates circulating immune markers in adults with obesity and either normal glucose (NG) or prediabetes, and the effects of a novel exercise intervention.
Results: The meta-analysis found that exercise was able to reduce liver fat by -2.4%, -3.13 to -1.66 (mean, 95% CI). In this randomised control trial study, people with prediabetes had increased liver fat compared to NG (absolute % liver fat in prediabetes: 11.4 ± 1.7, in NG: 5.2 ± 1.1, p= 0.002) despite having similar BMI at baseline. In a RCT involving a subgroup only of those in the PACE-G study, the exercise intervention (NG n=37, Prediabetes n=31), vs sham (NG n=39, Prediabetes n=29), showed a small effect on liver fat, which was not statistically significant when compared with control (NG exercise vs control: -0.7±0.7%, prediabetes exercise vs control: -1.2±0.9%). With respect to circulating cytokines IL-8 was significantly higher in NG than prediabetes and IL-15 and IL-22 were higher in prediabetes than NG. Interestingly, adults with prediabetes who undertook the exercise intervention did not realise the same reduction in pro-inflammatory cytokines as adults with NG. Finally, adults with prediabetes had reduced circulating angiogenic CD8+ T cells. Adults who undertook the exercise intervention improved circulating angiogenic T cells.
Conclusions: The work in this thesis shows that while only some types of exercise may improve metabolism and liver fat and novel CV risk markers may still be improved by certain exercise regimens even when metabolism is not overtly improved.
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Costa, Yuri Ajala da. "A proposal for full-range fat fraction estimation using magnitude MR imaging." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/18/18152/tde-01102018-083519/.
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Current methods for estimation of proton density fat fraction (PDFF) of the liver using magnitude magnetic resonance (MR) imaging face the challenge of correctly estimating it when fat is the dominant molecule, i.e. PDFF is more than 50%. Therefore, the accuracy of the methods is limited to half-range operation. We introduce a method based on neural networks for regression capable of estimating over the full range of fat fractions. We built a neural network based on the angles and distances between the data in the discrete MR signal (ADALIFE), using these as features associated to different PDFFs and as input for the network. Tests were performed assessing ADALIFE against dual echo, triple echo, and especially Multi-interference, a state-of-the-art method to estimate PDFFs, with simulated signals at various signal-to-noise (SNR) values. Results were compared in order to verify repeatability and agreement using regression analysis, Bland-Altman and REC curves. Results for Multi-interference were similar to its in-vivo literature, showing the relevance of a simulation. ADALIFE was able to correctly estimate fat fractions up to 100%, breaking the current paradigm for full-range estimation using only off-line post processing. Within half-range, our method outperformed Multi-interference in repeatability and agreement, with narrower limits of agreement and lower expected error at any SNR.Os métodos atuais para estimação de gordura hepática por densidade de prótons (PDFF) utilizando imagem de magnitude de ressonância magnética (RM) enfrentam o desafio de estimar corretamente quando a gordura é a molécula dominante, ou seja, PDFF é maior que 50%. Assim, a acurácia desses métodos é limitada a meio intervalo de operação. Apresentamos aqui um método baseado em redes neurais para regressão capaz de estimar pelo intervalo completo de frações de gordura. Construímos uma rede neural baseada nos ângulos e distâncias entre os dados do sinal discreto da imagem de RM (ADALIFE), usando esses atributos associados a diferentes valores de PDFF, com sinais simulados considerando diferentes relações sinal-ruído (SNR). Resultados foram comparados para verificar a repetibilidade e concordância através de análise de regressão, Bland- Altman e curvas de característica de erro de regressão (REC). Resultados para o método Multi-interferência (estado-da-arte) foram similares aos relatados in vivo pela literatura, ressaltando a relevância das simulações. ADALIFE foi capaz de estimar corretamente frações de gordura até 100%, quebrando o paradigma para intervalo completo de operação utilizando apenas processamento posterior à aquisição de imagens ou sinais. Considerando meio intervalo, nosso método superou o estado-da-arte em termos de repetibilidade e concordância, com limites mais estreitos e menor erro esperado em qualquer SNR.
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Kloock, Lisa [Verfasser], Michael [Gutachter] Roden, and Ulrich [Gutachter] Flögel. "The correlation of liver fat content and insulin resistance with skeletal muscle energy metabolism / Lisa Kloock ; Gutachter: Michael Roden, Ulrich Flögel." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/1136717900/34.
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Kloock, Lisa Verfasser], Michael [Gutachter] [Roden, and Ulrich [Gutachter] Flögel. "The correlation of liver fat content and insulin resistance with skeletal muscle energy metabolism / Lisa Kloock ; Gutachter: Michael Roden, Ulrich Flögel." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/1136717900/34.
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Elkatry, Haiam Omar Mohamed Verfasser], and Dietrich [Akademischer Betreuer] [Knorr. "Nonalcoholic fatty liver disease: Regulation of glucose and fat metabolism in the liver by Carbohydrate Response Element Binding Protein (ChREBP) and impact of dietary influence / Haiam Omar Mohamed Elkatry. Betreuer: Dietrich Knorr." Berlin : Universitätsbibliothek der Technischen Universität Berlin, 2011. http://d-nb.info/1016533543/34.
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Dillard, Kayla A. "Inclusion of Olive or Coconut Oil in a High-Fructose High-Fat Diet Increases Liver Injury in a Pig Model of Pediatric NAFLD." DigitalCommons@CalPoly, 2021. https://digitalcommons.calpoly.edu/theses/2308.
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Non-alcoholic fatty liver disease (NAFLD) represents the major cause of pediatric chronic liver pathology in the United States. The objective of this study was to investigate the effect of partial substitution of dietary lard by an isocaloric amount of olive or coconut oil on endpoints of NAFLD. Thirty-eight 15-d-old Iberian pigs housed in pens balanced for weight and sex were randomly assigned to receive 1 of 3 hypercaloric high-fructose high-fat (HFF) diets for 10 weeks: 1) lard (LAR; n=5 pens), 2) lard + olive oil (OLI, n=10), and 3) lard + coconut oil (COC; n=10). Additional pigs (BSL, n=4) were fed a eucaloric diet to establish baseline values. Animals were euthanized at 85 d of age after blood sampling. Liver tissue was collected for histology, metabolomics, and transcriptomics. Compared with BSL, OLI decreased high-density lipoproteins, phosphatidylcholines (PC), and total cholesterol in blood, and increased acylcarnitines in liver, whereas COC increased triacylglycerides (TAGs) in liver and blood. All HFF diets increased bile acids in liver, and decreased choline and fibroblast growth factor 19 in liver and blood. OLI and COC increased hepatic steatosis, necrosis, ballooning, and composite lesion score compared with LAR. OLI decreased gene expression of carnitine O-palmitoyltransferase 1, and COC increased expression of fatty acid binding proteins and acyl-CoA synthetase. In conclusion, partial replacement of dietary lard with olive and coconut oil dysregulated acylcarnitine metabolism and lipogenesis in the liver, increasing the severity of NAFLD in juvenile pigs.
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Cepero, Donates Yuneivy. "Pathogenic role of IL-15 in non-alcoholic fatty liver disease." Mémoire, Université de Sherbrooke, 2014. http://hdl.handle.net/11143/5871.
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Abstract : Pro-inflammatory cytokines play a key role in pathogenesis of obesity and non-alcoholic fatty liver disease (NAFLD). IL-15 is a pro-inflammatory cytokine, which signals through a receptor complex composed of the IL-15 receptor (IL-15R) alpha chain, the IL-2/IL-15R beta chain and the common gamma chain. The functions of IL-15 have been extensively described in immune cells but less is known about its functions in others tissues such as the liver. The aim of this thesis is to investigate the role of IL-15 in fatty liver disease.
C57BL/6 wildtype (WT) and IL-15 knockout (Il15[superscript -/-]) mice were maintained on high fat diet (HFD) or normal control diet (NCD). After 16 weeks, body weight, liver mass, fat accumulation in the liver, serum lipid levels and gene expression in the liver were evaluated. Intrahepatic lymphocytes (IHL) were also analysed. Primary hepatocytes were stimulated with IL-15 and chemokines gene expression was studied. IHLs were examined in WT, Il15[superscript -/-] and Il15ra[superscript -/-], as well as in macrophage- and hepatocyte-specific Il15ra[superscript -/-] mice.
We found that IL-15 deficiency prevents weight gain and accumulation of lipids in the liver. Circulating levels of cholesterol and non-esterified fatty acids were elevated in WT mice but not in Il15[superscript -/-] mice. Hepatic expression of chemokines such as Ccl2, Ccl5 and Cxcl10 was increased in WT mice under HFD, but not in Il15[superscript -/-] mice. The livers of Il15[superscript -/-] and Il15ra[superscript -/-] mice also showed decreased expression of Tnfa and iNOS, and macrophage markers Cd68 and F4/80. Accordingly, stimulation of primary hepatocytes with IL-15 induced chemokine gene expression in WT but not in Il15ra[superscript -/-] hepatocytes. Furthermore, hepatocyte-specific ablation of IL-15Rαreduced infiltration of NK and NKT cells in the liver, suggesting that IL15Rα expression in the hepatocytes is needed for the recruitment and/or maintenance of the NK cell population in the liver.
In conclusion, IL-15 promotes fat accumulation in the liver, and this is associated with increased inflammatory response in the liver. Increased availability of IL-15 in obesity may stimulate hepatocytes to secrete chemokines that promote hepatic inflammation resulting in fatty liver disease. IL-15Rα expression in hepatocytes appears to play a role in the maintenance of NK, NKT and iNKT cells. // Résumé : Les cytokines pro-inflammatoires jouent un rôle important dans la pathogenèse de l’obésité et la stéatose hépatique. L'IL-15 est une cytokine pro-inflammatoire qui est trans-présentée par l'IL-15Rα aux chaines IL-2/IL-15Rβ et γc. La fonction de l'IL-15 a été largement décrite dans les cellules immunitaires, mais ses fonctions dans d'autres tissus sont moins connues. Le but de ce mémoire est d'élucider le rôle de l'IL-15 dans la stéatose hépatique.
Les souris C57BL/6 de type sauvage (WT) et Il15[indice supérieur -/-] ont été soumises à un régimehyperlipidique (HFD) ou à un régime normal. Après 16 semaines, le poids corporel, lamasse hépatique, l'accumulation de lipides dans le foie, les taux de lipides sériques et l'expression des différents gènes reliés à l’inflammation et au métabolisme dans le foie ont été évalués. Les lymphocytes intra-hépatiques (IHL) ont été également étudiés. Des hépatocytes primaires ont été stimulés avec IL-15, et l'expression génique de chimiokines a été déterminée. Les populations de IHLs ont été également caractérisées chez les souris WT, Il15[indice supérieur -/-] et Il15ra[indice supérieur -/-], ainsi que chez des souris dont la déficience dans l’expression d’IL-15Rα est ciblée aux macrophages ou aux hépatocytes.
Nos résultats montrent que la déficience en IL-15 empêche l'accumulation de lipides dans le foie. Les taux de cholestérol et d’acides gras non estérifiés dans le sang étaient élevés chez les souris WT, mais pas chez les souris Il15[indice supérieur -/-]. L'expression hépatique des chimiokines Ccl2, Ccl5, Cxcl10 et des marqueurs de macrophages était augmentée chez les souris WT sous HFD, mais pas chez les souris Il15[indice supérieur -/-]. La stimulation des hépatocytes primaires avec l'IL-15 induit l'expression des gènes des chimiokines chez les hépatocytes WT, mais pas chez les Il15ra[indice supérieur -/-]. En outre, nous avons trouvé une infiltration réduite des
cellules NK et NKT dans le foie des souris déficientes en Il15ra[indice supérieur -/-] dans les hépatocytes, ce qui suggère que l'expression d’IL15Rα chez les hépatocytes est nécessaire aurecrutement des cellules NK, NKT et / ou à leur maintien.
En conclusion, nous proposons que l’IL-15 favorise l'accumulation de lipides dans le foie,
et que ceci est associée à une réponse inflammatoire accrue. La disponibilité accrue de
l'IL-15 dans l'obésité pourrait stimuler les hépatocytes à secréter des chimiokines ce qui
favorise l'inflammation hépatique et conduirait à la stéatose hépatique. L’expression de
l'IL-15Rα dans les hépatocytes semble jouer un rôle principal dans l’infiltration des
cellules NK, NKT et iNKT dans le foie.
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Berglund, Johan. "Separation of Water and Fat Signal in Magnetic Resonance Imaging : Advances in Methods Based on Chemical Shift." Doctoral thesis, Uppsala universitet, Enheten för radiologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-158111.
Full textAbstract:
Magnetic resonance imaging (MRI) is one of the most important diagnostic tools of modern healthcare. The signal in medical MRI predominantly originates from water and fat molecules. Separation of the two components into water-only and fat-only images can improve diagnosis, and is the premier non-invasive method for measuring the amount and distribution of fatty tissue. Fat-water imaging (FWI) enables fast fat/water separation by model-based estimation from chemical shift encoded data, such as multi-echo acquisitions. Qualitative FWI is sufficient for visual separation of the components, while quantitative FWI also offers reliable estimates of the fat percentage in each pixel. The major problems of current FWI methods are long acquisition times, long reconstruction times, and reconstruction errors that degrade image quality. In this thesis, existing FWI methods were reviewed, and novel fully automatic methods were developed and evaluated, with a focus on fast 3D image reconstruction. All MRI data was acquired on standard clinical scanners. A triple-echo qualitative FWI method was developed for the specific application of 3D whole-body imaging. The method was compared with two reference methods, and demonstrated superior image quality when evaluated in 39 volunteers. The problem of qualitative FWI by dual-echo data with unconstrained echo times was solved, allowing faster and more flexible image acquisition than conventional FWI. Feasibility of the method was demonstrated in three volunteers and the noise performance was evaluated. Further, a quantitative multi-echo FWI method was developed. The signal separation was based on discrete whole-image optimization. Fast 3D image reconstruction with few reconstruction errors was demonstrated by abdominal imaging of ten volunteers. Lastly, a method was proposed for quantitative mapping of average fatty acid chain length and degree of saturation. The method was validated by imaging different oils, using gas-liquid chromatography (GLC) as the reference. The degree of saturation agreed well with GLC, and feasibility of the method was demonstrated in the thigh of a volunteer. The developed methods have applications in clinical settings, and are already being used in several research projects, including studies of obesity, dietary intervention, and the metabolic syndrome.
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Bellenzani, Marcela Palomo Pieroni 1984. "Expressão de enzimas envolvidas na produção de triacilglicerol em tecidos adiposo e hepático isolados de ratos normo e hiperlipidêmicos." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314094.
Full textAbstract:
Orientador: Dora Maria Grassi KassisseDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-20T14:23:50Z (GMT). No. of bitstreams: 1 Bellenzani_MarcelaPalomoPieroni_M.pdf: 6472856 bytes, checksum: e473a96a17b23ee1d9a456d9ac7a4602 (MD5) Previous issue date: 2012
Resumo: A pandemia da obesidade é evidente no início do século XXI. O fator desencadeante mais relevante é a alimentação hipercalórica associada ao sedentarismo. Modelos de estudo em ratos para investigar as etapas que precedem o desenvolvimento desta doença são fundamentais para propor terapias de prevenção. No modelo de indução da dislipidemia pela dieta por quatro semanas, os ratos apresentam hipercolesterolemia, hipertrigliceridemia e hiperinsulinemia e com seis semanas de administração da dieta observa-se um aumento no peso dos panículos adiposos da região epididimal e peri-renal e sem alteração no depósito da região mesentérica. Assim sendo, objetivamos, nesta tese, analisar as vias metabólicas envolvidas no processo de metabolização da glicose e triacilgliceróis nos tecidos adiposo branco e hepático em ratos hiperlipidêmicos e para tal estudamos as vias lipogênica, lipolítica e neoglicogênica, pela quantificação da expressão gênica das enzimas chaves envolvidas nestes processos. A dislipidemia foi induzida pelo oferecimento de dieta hiperlipídica (grupo dieta, D) ao longo de quatro semanas a ratos jovens e a instalação do quadro foi verificada pelas análises plasmáticas ao final do tratamento e após jejum de 16h. Amostras de tecidos hepático e adiposo foram coletadas para análise histológica e quantificação da expressão gênica sendo estas analisadas por qRT-PCR. Observou-se que ratos que ingerem dieta hiperlipídica (+129+10,13 g) ganham peso de forma semelhante aos ratos controle (C: +148+8,8 g) mesmo ingerindo quantidade significativamente menor de dieta (C: 20,8+0,62 g vs D: 14,87+0,66 g). As análises histológicas ilustram aumento no teor de depósitos de lipídeos no tecido hepático. A expressão gênica no tecido hepático de ratos dieta foi aumentada significativamente para as enzimas lipoproteína lipase, piruvato desidrogenase quinase 4 e fosfofrutoquinase 1 e diminuição significativa na expressão de glicose 6-fosfatase sem alteração na quantificação da expressão de acetil-CoA carboxilase alpha, gliceroquinase, piruvato desidrogenase fosfatase 2. Em relação ao tecido adiposo observamos que a expressão das enzimas acetil-CoA carboxilase e piruvato desidrogenase fosfatase 2 não foi significativamente alterada em nenhum dos depósitos adiposos. A lipase hormônio-sensível não apresentou alterações no tecido adiposo epididimal, porém teve sua expressão significativamente aumentada nos tecidos mesentérico e peri-renal. A expressão da lipoproteína lipase por sua vez, não se alterou no panículo adiposo epididimal nem no panículo adiposo mesentérico estando diminuída no panículo adiposo peri-renal. E por fim, a piruvato desidrogenase quinase 4 também não apresentou alterações nos depósitos epididimal e mesentérico porém no peri-renal sua expressão encontrou-se aumentada. Estes resultados, em conjunto, indicam que a dieta administrada por 4 semanas, mesmo não apresentando todas as alterações observadas com 6 semanas, pode ser útil para os estudos iniciais do quadro de dislipidemia que antecedem as disfunções metabólicas
Abstract: The pandemic of obesity is evident in the twenty-first century. The most important and triggering factor is the high-calorie diet associated with physical inactivity. Study models in rats to investigate the steps that precede the development of this disease are essential to propose preventive therapies. In the model of induction of dyslipidemia by diet for four weeks, the mice exhibit hypercholesterolemia, hypertriglyceridemia, and hyperinsulinemia and there is an increase in weight of the panniculus region of epididymal and peri-renal depot and no change in the mesenteric region. Therefore, we aimed to analyze the metabolic pathways involved in the metabolism of glucose and triglycerides in white adipose tissue, and liver in hyperlipidemic rats and to study the ways that lipogenic, lipolytic and glyconeogenic for the quantification of gene expression of key enzymes involved in these processes. Dyslipidemia was induced by offering high-fat diet (diet group, D) over four weeks to young rats and onset of condition was verified by analysis at the end of the plasma treatment and after fasting for 16 hours. Samples of liver and adipose tissue were collected for histological analysis and quantification of gene expression and these were analyzed by qRT-PCR. It was observed that mice eat high-fat diet (+129 +10.13 g) gain weight similarly to control rats (C: +8.8 +148 g) even eating significantly less diet (C: 20.8 +0.62 g vs D: 14.87 +0.66 g). Histological analysis illustrate the content of lipid deposits in liver tissue. Gene expression in liver tissue of rats diet was significantly increased for the enzymes lipoprotein lipase, pyruvate dehydrogenase kinase 4 and 1 and Phosphofructokinase significant decrease in the expression of glucose 6-phosphatase no change in the quantification of the expression of acetyl-CoA carboxylase alpha, Gliceroquinase, pyruvate dehydrogenase phosphatase 2. In relation to the adipose tissue we observed that the expression of the enzyme acetyl-CoA carboxylase and pyruvate dehydrogenase phosphatase 2 was not significantly altered in any of the fatty deposits. The hormone-sensitive lipase showed no changes in epididymal adipose tissue but its expression was significantly increased in mesenteric tissue and peri-renal. Lipoprotein lipase, in turn, did not change in the mesenteric or epididymal being reduced in the peri-renal. And finally, the pyruvate dehydrogenase kinase 4 also showed no changes in epididymal and mesenteric but the peri-renal expression is increased. These results, together, indicate that the diet for 4 weeks, even not showing all changes observed within 6 weeks, can be useful for the initial studies of hyperlipidemia that precede the metabolic dysfunctions
Mestrado
Fisiologia
Mestre em Biologia Funcional e Molecular
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Patton, Ashley. "Characterization of the Very Early Development of High Fat Diet-induced Non-alcoholic Fatty Liver Disease (NAFLD) and Efficacy of Novel Therapeutics for its Treatment." Ohio University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1521811677550828.
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Cattelam, Jonatas. "Caraterísticas pós-abate de bovinos terminados com substitutos ao milho em dietas de alto grão." Universidade Federal de Santa Maria, 2015. http://repositorio.ufsm.br/handle/1/4375.
Full textAbstract:
Coordenação de Aperfeiçoamento de Pessoal de Nível SuperiorThe objective of this study was to evaluate the characteristics of non-integrant parts of steers and heifers, feedlot fed with high-grain diets. Were used forty-five cattle were used in two categories, with 21 heifers with initial age of 32 months and 24 steers with initial age of 20 months, from the crossing between Charolais and Nellore. The animals were assigned to treatments as according energy source in the diet, being these: rice; white oat or corn, being seven heifers and eight bulls for each diet. The animals were confined until, by estimate, hot carcass weight of 220 kg. A complety randomized experimental design was completely randomized in 3 x 2 factorial arrangement (three food treatments and two categories). Slaughter weights were higher for cattle fed with white oat (449.3 kg) or corn (430.4 kg) compared to animals that receiving rice (401.8 kg), with higher carcass yields for animals than received corn. For the relationship between the empty body weight and slaughter weight of cattle also was no difference between the diets used and the major relationship was observed for animals that received corn (88.3%) compared to animals fed with rice (84.9%) or oat (84.1%). The exception of heart fat, in different forms of expression, and abomasal fat, expressed in relation to the empty body weight, for the remaining fat deposits, animals fed rice showed lower values. Regarding of animal category, the steers showed greater development of internal organs in different expression forms and legs and total of peripheral components, expression in relation to the empty body weight, while heifers showed higher weight for omasum and higher deposition in total fat. Weights and yields of commercial cuts sidecut and sawcut were higher for cattle fed with white oat or corn. For the forequarter weight and arm circumference, animals that received corn were higher than the animals that received rice, with intermediate behavior for cattle fed with white oat. Animals that received rice showed tenderness (5.15 points) and palatability (5.46 points) lower compared those were fed white oat (5.73 and 6.40 points, respectively) or corn (6.04 and 6.45 points, in the same order). According as the animal categories, steers showed higher percentage of forequarter (38.00 against 37.4%), while heifers showed greater carcass length (126.0 against 123.1 cm). The use of high-grain diets based on corn or white oat in finishing cattle results in a higher development of internal organs and the digestive tract, produce carcasses with higher weight and adequate fat deposition and with higher yields of commercial cuts, while feeding with rice produce lean meats, however reduces the carcass weight, with higher chilling loss and less tenderness meat. The production of heifers or steers feedlot finished ensures similar organleptic meat products.
O presente estudo teve por objetivo avaliar as características pós-abate de novilhos e novilhas, terminados em confinamento alimentados com dietas de alto grão. Utilizaram-se 45 bovinos de duas categorias, sendo 21 novilhas com idade inicial de 32 meses e 24 novilhos com idade inicial de 20 meses, oriundos do cruzamento entre as raças Charolês e Nelore. Os animais foram distribuídos nos tratamentos conforme a fonte energética utilizada na dieta, sendo essas: arroz; aveia branca ou milho, sendo utilizados sete novilhas e oito novilhos para cada dieta alimentar. Os animais permaneceram confinados até atingir, por estimativa, peso de carcaça quente de 220 kg. O delineamento experimental foi o inteiramente casualizado, com arranjo fatorial 3 x 2 (três tratamentos alimentares e duas categorias de bovinos). Os pesos de abate foram superiores para os bovinos alimentados com aveia branca (449,3 kg) ou milho (430,4 kg) em relação aos animais que receberam arroz (401,8 kg), com maiores rendimentos de carcaça para os animais que receberam milho. Para a relação entre os pesos de corpo vazio e de abate dos bovinos também ocorreu diferença entre as dietas alimentares utilizadas sendo que a maior relação foi observada para os animais que receberam milho (88,3%) comparada aos animais alimentados com arroz (84,9%) ou aveia branca (84,1%). A exceção das gordura de coração, nas diferentes formas de expressa, e da gordura abomasal expressa em relação ao peso de corpo vazio, para os demais depósitos de tecido adiposo, os animais alimentados com arroz apresentaram menores valores. Com relação a categoria animal, os novilhos apresentaram maior desenvolvimento dos órgãos internos nas distintas formas de expressão, e das patas e total de componentes periféricos expressos em relação ao peso de corpo vazio, enquanto as novilhas apresentaram maior peso de omaso e maior deposição no total de gorduras. Os pesos e rendimentos dos cortes comerciais costilhar e serrote foram superiores para os bovinos que receberam aveia branca ou milho. Para o peso de dianteiro e perímetro de braço, animais que receberam milho foram superiores aos animais que receberam arroz, com comportamento intermediário para os bovinos que receberam aveia branca. Animais que receberam arroz apresentaram maciez (5,15 pontos) e palatabilidade (5,46 pontos) inferiores em relação aqueles que foram alimentados com aveia branca (5,73 e 6,40 pontos, respectivamente) ou milho (6,04 e 6,45 pontos, citados na mesma ordem). Quanto as categorias animais avaliadas, novilhos apresentaram maior rendimento de dianteiro (38,00 contra 37,4%) ao passo que novilhas demonstraram maior comprimento de carcaça (126,0 contra 123,1 cm). A utilização de dietas de alto grão a base de milho ou aveia branca na terminação de bovinos acarreta em maior desenvolvimento de órgãos internos e do trato digestório, produz carcaças mais pesadas, com adequada deposição de gordura e com melhor rendimento dos cortes principais da carcaça enquanto a alimentação com arroz em dietas de alto grão produz carnes mais magras, porém reduz o peso de carcaça, com maior perda ao resfriamento e carne de menor maciez. A produção de novilhas ou novilhos confinados assegura produtos cárneos de qualidades organolépticas similares.
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Scanlon, Jessica Patricia. "High fat diet has sexually dimorphic effects on body composition, adiposity and glucose homeostasis in Poly(A)-binding protein 4 (Pabp4) knockout mice." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28893.
Full textAbstract:
Obesity can lead to a range of health problems including type 2 diabetes (T2DM), cardiovascular disease and non-alcoholic fatty liver disease (NAFLD), and causes an estimated 2.8 million deaths annually (2016). It is a growing epidemic affecting over 600 million people worldwide (in 2014), with 26.8% of the adult population in England alone being obese, an increase of 10% in the last decade, and 62.9% overweight or obese. This trend is predicted to continue, and is attributed to an increasingly sedentary lifestyle, coupled with a high calorie “western diet”, which is estimated to cost >£25billion/year in the UK (2015), which is predicted to rise to £49.9 billion by 2050. It is clear that both sex and genetics affect the extent to which individuals exposed to a high fat diet develop adiposity and its associated morbidities, although the mechanisms underlying these differences are not well understood. Here we explore this aetiology, focusing on poly(A)-binding protein 4 (PABP4), an RNA-binding protein in which polymorphisms associated with altered cholesterol levels and cardiovascular disease risk were identified in human GWAS studies. To this end, I take advantage of an unpublished Pabp4 knock-out mouse, maintained on either normal (ND) or high fat diet (HFD), to explore the role of PABP4 in determining the response to high fat diet. PABP4 is a poorly characterised member of the PABP family, which are multifunctional central regulators of global and mRNA-specific translation, and stability. In cell lines, PABP4 is predominantly cytoplasmic, consistent with such functions. However, analogously to PABP1, the prototypical PABP family member, PABP4 is relocalised to stress granules or the nucleus in response to specific cellular stresses and/or viral infections, suggesting a role in altering gene expression programs in responses to changing cellular conditions. Whilst the expression pattern of PABP4 within tissues has not been previously characterised, western blotting of adult mouse tissues revealed that PABP4 is highly expressed in tissues relevant to obesity, T2DM and NAFLD, such as adipose, pancreas, liver and muscle, consistent with the idea that it may play a role in regulating gene expression programs in response to HFD. Immunohistochemistry of tissue sections provided additional insight, revealing a distinct cellular distribution of PABP4 in some tissues, when compared to the well characterised PABP1. Birth weight and post-birth growth can affect adult metabolism. In particular, low birth weight and catch-up growth, characterised by preferentially putting down adipose over lean mass, increases the risk of metabolic conditions in adulthood, such as obesity, T2DM and cardiovascular disease. Therefore, Pabp4-/- and wildtype mice were weighed at birth and daily until weaning. Interestingly this revealed that Pabp4-/- mice have a reduced weight at birth that is exacerbated to weaning (21days (P21)) (5.7% and 18.3% reductions respectively). This analysis also uncovered a reduced survival to weaning, with both male and female Pabp4-/- mice being present at sub-Mendelian ratios by P21 (p=0.0056). Whilst most death occurred neonatally, Pabp4-/- mice showed an increased rate of attrition until weaning, preceded in some cases by an arrest of weight gain. Weight gain was also tracked from 4 weeks to 12 weeks of age on normal diet showing that Pabp4-/- mice had reduced weight into adulthood (12% reduction at 12wks). Analysis of weight gain by sex uncovered a sexually dimorphic effect of Pabp4-deficiency, with female, but not male, Pabp4-/- mice remaining reduced in weight compared to wildtype after 8 weeks on ND (13.4% reduction in female weight). Body composition analysis showed that fat mass was equivalent to wildtype at 12 weeks of age in both sexes but that female Pabp4-/- mice had a 14.3% reduction in lean mass. Neither the catch-up growth in males nor the reduced lean mass in females was sufficient to result in a change in glucose homeostasis. As the risk of developing metabolic disorders in adult life is a consequence of both genetic and environmental factors, such as diet, Pabp4-/- were placed on a HFD at 4 weeks of age for 8 weeks. HFD models the ‘western’ diet, and has been shown to induce obesity, insulin resistance and glucose intolerance in wildtype mice. Whereas Pabp4-/- mice were only distinguishable from wild-type in terms of female lean mass on normal diet, pronounced sexually dimorphic differences were observed in HFD fed mice. Male Pabp4-/- mice appeared to be partially protected from the negative effects of an 8 week HFD regimen, with a 44% decrease in adipose mass gain compared to wildtype despite equal lean mass. Pabp4-/- male mice also had significantly reduced ectopic lipid stores, with an 81% decrease in hepatic triglyceride concentration compared to wildtype, meaning that NAFLD has not developed. Furthermore, Pabp4- /- male mice did not develop hyperinsulinemia on HFD and retained insulin sensitisation (assessed via glucose tolerance test (GTT) and insulin tolerance test (ITT)), although they displayed wildtype-like elevated plasma glucose concentrations (compared to ND). Western blotting had detected high PABP4 levels in the pancreas, indicating a possible pancreatic origin of these alterations. However, immunofluorescence revealed that PABP4 was confined to the exocrine portion of the pancreas, and was undetectable in the insulin producing pancreatic beta cells, suggesting this phenotype may not be beta cell in origin. This is consistent with the fact that the Pabp4-/- male mice retained an appropriate glucose-induced burst of insulin secretion, and therefore insulin production appears unimpaired. Thus, the primary defect may reside in the exocrine pancreas, which aids digestion, or in other key metabolism related tissues (e.g. muscle, liver, adipose and brain), or a combination thereof. In HFD fed wildtype mice, insulin resistance is caused by increased adiposity and ectopic lipid depots, which blunt insulin stimulated signalling cascades, meaning that the normal responses to insulin (e.g. cellular up take of glucose in muscle and arrested glucose production in liver, to decrease plasma glucose concentrations), are impaired. Therefore, the absence of insulin resistance in HFD fed Pabp4-/- male mice may be a consequence of the reduced increase in adipose mass and ectopic lipid deposits detected in these mice, and their consequent lack of inhibition on insulin signalling pathways. The reduced adiposity was not a result of reduced food intake or dietary fat absorption as male Pabp4-/- mice did not eat less nor exhibit apparent steatorrhea (fatty stools). These results highlight that the Pabp4-/- male mice appear to have an alteration in energy use/storage, and the investigation of this will form the basis of future work. When fed HFD, female Pabp4-/- mice revealed a divergent phenotype to that of wildtype female mice and Pabp4-/- male mice. HFD fed Pabp4-/- female mice showed no difference to HFD-fed wildtype mice in terms of weight, but still exhibited the reduction in lean mass seen on ND, but now with a 22.8% increase in volume of adipose tissue. Together, this means that HFD fed Pabp4-/- females have a higher body fat percentage (32.6% compared to 25.9 % for wildtype females). In contrast to the males, there was no difference in terms of hepatic triglycerides in HFD fed Pabp4-/- female mice and they showed greater hyperglycaemia than wildtype (GTT), although like males they retained insulin sensitisation (ITT). These potentially conflicting results in terms of insulin sensitivity and plasma glucose concentrations may result from the alterations in body composition, which can confound results when lean mass is altered and total body weight is used for calculating doses for GTT/ITT. Interestingly, adiponectin, an adipokine normally found in inverse proportion to adipose mass, was increased in plasma from HFD fed Pabp4-/- female mice (21% increase from HFD fed wildtype mice). Whilst surprising given the increase fat mass of Pabp4-/- females, the insulin sensitising properties of adiponectin may help to explain the retained insulin sensitivity detected in the female Pabp4-/- mice.The finding that HFD revealed metabolic differences in the Pabp4-/- mice lead to the question of whether Pabp4-/- mice have issues adapting to other situations which require modulation of energy storage and glucose homeostasis. One such event is pregnancy, when maternal regulation of insulin resistance is tightly modulated throughout gestation. We therefore characterised the maternal Pabp4-/- environment in late pregnancy (E18.5), when insulin sensitivity decreases to 40-60% lower than pre-pregnancy which results reduced maternal glucose uptake, freeing the glucose up for the rapidly developing foetus. Pregnant Pabp4-/- mice had elevated plasma insulin concentration post fasting (63.7% increase), however glucose homeostasis was wildtype-like, both in terms of plasma glucose and insulin concentrations, throughout a GTT. However, plasma glucose and insulin concentrations in E18.5 Pabp4-/- foetuses were significantly decreased (9% and 44.3% respectively). Pabp4-/- foetuses also had reduced foetal and placental weight/length parameters. This establishes that the differences in weight observed at birth were present by late gestation and secondly, that the reductions in both foetal glucose and insulin concentrations which may contribute to or underlie the reduced growth. It also suggests that the differences seen in adulthood on HFD may be a consequence of metabolic differences present during pregnancy. Taken together, these data support the hypothesis that PABP4 plays a key role in the regulation of mRNAs which are important in growth, post-natal survival and metabolic adaption to high fat diet.
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Ko, Wei-Huei, and 柯蘊慧. "The correlation between body fat, visceral fat and nonalcoholic fatty liver disease." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/13572316414529343756.
Full textAbstract:
碩士臺北醫學大學
公共衛生學系暨研究所
104
Objective: The aim of this study is to investigate the correlation between body fat, visceral fat and presence of nonalcoholic fatty liver disease(NAFLD). Design: It is a cross-sectional study. Subjects: We collected data from physical examination subjects at Renai Branch of Taipei City Hospital from October 2013 to September 2015. The enrolled criteria required participants be 20 years or older. All subjects those with liver disease(hepatitis C virus antibody or hepatitis B surface antigen)or cirrhosis or malignant disease or biliary disease or use of antihypertensive or antidiabetic agents were excluded. Methods: Demographic data, biochemical data, body fat, visceral fat, fatty liver were collected by chart review. Body fat and visceral fat assessed by InBody 720 (Biospace, Seoul, Korea). Fatty liver was diagnosed by abdominal ultrasound. SPSS software version 21.0 was used to perform statistical analyses. A p value less than .05 was considered as statistic significance. Results: A total of 2,759 subjects were collected this study. The result of the analysis revealed that in terms of prevalence of NAFLD males exhibited a higher incidence than females. Those factors such as waist circumference, body mass index, body fat, visceral fat and metabolic syndrome were correlation with NAFLD. Multiple logistic regression was used in further analysis, showing that increased waist circumference, body mass index, body fat, visceral fat and metabolic syndrome were significant correlated factors for the present of fatty liver. Receiver operating characteristic suggested that visceral fat cut off point was 70.5 cm²(Youden''s index=0.4352). Conclusion: Visceral fat was a strong predictor of NAFLD.
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Ribeiro, Mário J. P. "Fat quantification in liver using chemical shift imaging." Master's thesis, 2013. http://hdl.handle.net/10316/25143.
Full textAbstract:
MRI is becoming increasingly important in the characterization of NAFLD,
which is one of the most relevant di use liver diseases with increasing prevalence
in the developed countries. Currently, biopsy is the gold standard in the
early identi cation and staging of NAFLD, which is crucial to evaluate the risk
of hepatocellular carcinoma development. However, the later is associated with
sampling errors and with the development of several post-surgical complications.
In this work, we address the problem of quantifying the fat accumulation
in the liver using a non-invasive procedure based on chemical shift imaging and
two signal models, the magnitude and complex models. In particular, we address
the in
uence of noise, relaxation e ects and choice of echo times in fat
fraction estimation error. Our approach relied in the development of a new
acquisition strategy based on the optimal choice of echo times, which were
evaluated in simulation studies and later tested with phantoms. A program to
perform in-vivo fat quanti cation was implemented, extending our approach to
clinical data. Results indicate that good fat fraction estimation can be achieved
by correctly choosing the echo times. However, it is extremely di cult to nd a
single echo time combination which optimize a large range of fat fractions. Finally,
we also demonstrate that the standard clinical protocol has several
aws
and that a new acquisition protocol must be developed.
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Hsin-YingLin and 林欣盈. "Effects of galactose on fat metabolism in mice liver." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/6t8mqs.
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TRAN, VAN-BIEN, and 陳文邊. "Application of Dixon method to study the correlation between liver fat content and types of liver disease." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/95456670675831987570.
Full textAbstract:
碩士元培醫事科技大學
醫學影像暨放射技術系碩士班
104
Generally, human liver fat content is about 5-10%. When the liver is disturbed, fat content changes. There are many fat content inspection techniques, including biopsies, ultrasound (US), computed tomography (CT) and magnetic resonance imaging (MRI). Among these techniques, MRI is a non-invasive and no-radiation choice that possesses high sensitivity and specificity characteristics, though fairly costly. In this retrospective study, we collected water-only and fat-only images of 260 subjects (20-90 years), each of whom had already undergone the Dixon method measurement of their abdomens with a GE 1.5T MRI scanner, from January 2013 to July 2015. On each liver image, three circled regions of interest (ROI) with same volume were chosen to make sure of the homogeneity of these ROIs. The averaged fat-to-water ratios were then calculated for fat content of the liver in each subject. Concurrently, the types of liver disease in these subjects were classified into several groups. Finally, SPSS 20.0 statistical software was used for analysis. Our results showed significant differences in liver fat content among the age groups (p<0.05). Fat content in the 41- 60 age group (15%) is higher than the other two groups (20-40 at 10-11%; 61-90 at 12-14%). In addition, the fat content of the fatty liver group was 33%, and of the general liver disease, non-fatty liver group was 10-15%. The Pearson correlation analyses about with and without fatty liver in both male and female showed moderate to high correlations (p<0.001) regardless of malignant or benign disease. From this study and previous analyses in our group, we found the commercial Dixon method is likely not good enough for fat content quantification. For routine use in clinical studies in the future, it may need further optimization to avoid respiratory artifacts and signal phase problems
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Hoe, Teck-Loong, and 胡德龍. "Lignosus rhinocerus attenuated high fat diet induced non-alcoholic fatty liver." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/09348138734810047733.
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Chiu, Jian-Jia, and 邱健佳. "Assessment of Liver Fat With T2 Correction Using Magnetic Resonance Spectroscopic Image." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/50264668570634093508.
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碩士國立臺灣科技大學
電子工程系
100
Early detection of non-alcoholic fatty liver disease (NAFLD) can prevent further complications such as steatohepatitis, fibrosis and cirrhosis. Currently quantification of liver fat content relies on liver biopsy which is highly invasive method is still the gold standard for the evaluation of hepatic steatosis, but invasive method had a lot of disadvantages. Noninvasive study will become important. For noninvasive, magnetic resonance spectroscopy (MRS) and magnetic resonance imaging (MRI) are the good methods in lipid content test. There had a lot of outstanding research in MRS, But there focused in single voxel spectroscopy (SVS). In previous study, we used a fast magnetic resonance spectroscopic imaging (MRSI) techniques, acquisition sequence is proton echo-planar spectroscopic imaging (PEPSI) to measure lipid fat content. PEPSI is able to detect spatial distribution, and this is a fast acquisition sequence. In this thesis, we further investigated the influence of T2 relaxation effects. PEPSI scans with different TE were repeated 8 times to observe the reproducibility of T2 correction. Our results showed that the measured fat content is highly reproducible and the liver lipid T2 range is wide, so T2-correction is necessary in fat content quantified.
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Liao, Chung-Chia, and 廖重佳. "Effects of Phenolic Acid on Body Fat, Fatty Liver and Bladder Cancer." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/64001795466210134686.
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博士中山醫學大學
生化暨生物科技研究所
104
Caffeic acid (CA) can inhibit toxin-induced liver injury. In this study, CA is assessed for its lipid lowering potential when oleic acid is used to induce non-alcoholic fatty liver disease in human HepG2 cells. The results showed that both the triglyceride and cholesterol content are decreased in the HepG2 cells by using the enzymatic colorimetric method. CA enhances the phosphorylation of AMP-activated protein kinase (AMPK) and its primary downstream target enzyme, acetyl-CoA carboxylase. CA down-regulates the lipogenesis gene expression of sterol regulatory element-binding protein-1 and its target genes through AMPK activation. C57BL/6 mice were fed a normal diet or a HFD (20% fat) with or without caffeic acid for 6 weeks. The supplementation of caffeic acid significantly lowered body weight, visceral fat mass, plasma GOT and GPT levels, FAS activity, and free fatty acid compared to the HFD group. Caffeic acid also lowered triglyceride and cholesterol concentrations in plasma and liver. Gallic acid (GA) has been shown to inhibit carcinogenesis in animal models and various cancer cell lines. The TSGH-8301 bladder cancer cell line was treated with different concentrations of gallic acid. It showed that GA inhibited TSGH-8301 bladder cancer cell proliferation via the PI3K/Akt and MAPK/ERK pathway. Our results showed that GA decreased Skp2 protein level and attenuated Skp2-p27 association. It is suggested that gallic acid acts upstream of the proteasome to control p27 levels and ultimately inhibits G2/M phase transition. Our study showed that GA suppressed bladder cancer cell invasion and migration through RhoB/p-AKT/p-IkB/NF-kB/MMP-2 signaling pathway. GA also increased ER alpha expression, which prevented bladder cancer in animal study. GA decreased FAS protein level in our study. It is possible that gallic acid inhibited TSGH-8301 bladder cancer cell growth, invasion and migration through inhibition of fatty acid synthase.
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Long, Michelle. "Association between alcohol use behavior and liver fat in the Framingham Heart Study." Thesis, 2019. https://hdl.handle.net/2144/36033.
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Many individuals presumed to have non-alcoholic fatty liver disease (NAFLD) consume moderate amounts of alcohol; however, little is known regarding patterns of alcohol use and how drinking behaviors may influence liver fat. We conducted a cross-sectional study of 2,475 participants of the Framingham Heart Study who underwent computed tomography (CT) to define liver fat. We performed multivariable-adjusted logistic regression models for the association between different alcohol drinking patterns, including the average alcoholic drinks/week, frequency of alcohol use, usual quantity of alcohol consumed, maximum drinks consumed in 24 hours, and binge drinking behavior, and CT-defined hepatic steatosis. We excluded heavy alcohol users defined as women who drink > 14 drinks/week and men who drink > 21 drinks/week. We also performed an analysis specific to beverage type (beer, wine, or liquor/spirit drinks).The prevalence of hepatic steatosis in our study sample (mean age ± standard deviation (SD) 49.8±10.2, 50.3% women) was 17.5%. Among individuals with presumed NAFLD, binge drinking occurred in 25.4% of individuals. In adjusted models, the odds of hepatic steatosis increased by 20% for each SD increase in the number of alcoholic drinks consumed per week (OR 1.20; 95% confidence interval (CI) 1.08, 1.36). Frequency of alcohol use (drinking days/week) was also associated with hepatic steatosis (OR 1.09; 95% CI 1.03, 1.15). The odds of hepatic steatosis increased by 15% for each SD increase in the maximum drinks per week (OR 1.15; 95% CI 1.02, 1.30). In the beverage specific analysis, alcohol use patterns were associated with hepatic steatosis among beer drinkers, but no significant associations were observed among wine drinkers. Conclusions: Even after excluding heavy alcohol users from our sample, alcohol use contributed to liver fat, which suggests alcohol-related liver fat may be present among individuals presumed to have NAFLD. Additional prospective studies are needed to validate our findings and to determine if more comprehensive alcohol use screening tools should be used in practice or clinical trial settings.2020-06-03T00:00:00Z