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Samra, Jaswinder Singh. "Regulation of fat mobilisation in normal subjects in the post-absorptive state : role of hormones." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319044.
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Farré, Guasch Elisabet. "Adipose Stem Cells from Buccal Fat Pad and Abdominal Adipose Tissue for Bone tissue Engineering." Doctoral thesis, Universitat Internacional de Catalunya, 2011. http://hdl.handle.net/10803/31987.
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ABSTRACT
Background and Objective: Stem cells offer an interesting tool for tissue engineering, but the clinical applications are limited by donor site morbidity and low cell number upon harvest. Recent studies have identified an abundant source of stem cells in subcutaneous adipose tissue. These adipose stem cells (ASC), are able to differentiate to several lineages and express multiple growth factors, which makes them suitable for clinical application. Buccal fat pad (BFP), an adipose encapsulated mass in the oral cavity, could represent an easy access source for dentists and oral surgeons. Biosynthetic substitutes such as β-tricalcium phosphate (β-TCP), hydroxyapatite (HA), and mixtures of HA/β-TCP (biphasic calcium phosphate; BCP) have been successfully used as bone graft biomaterials. Growth factors stimulating osteogenic differentiation are also interesting for bone tissue engineering applications. We aimed to investigate whether BFP is a rich source of ASC, and whether ASC triggered for only 15 min with bone morphogenetic protein-2 (BMP-2), and seeded onto different calcium phosphate scaffolds composed of β-TCP alone or mixtures of HA/β-TCP, could stimulate bone formation.
Materials & Methods: ASC obtained from subcutaneous abdominal adipose tissue and BFP were counted and analyzed by flow cytometry, to determine ASC cell number, phenotype and percentage. At two weeks of culture, the multipotent differentiation potential of ASC from BFP was analyzed. Furthermore, fresh ASC either or not stimulated with 10ng/ml BMP-2 for 15min were seeded on different calcium phosphate scaffolds. ASC attachment, proliferation and osteogenic differentiation was analyzed and compared.
Results: BFP contained ~30% of ASC. The ASC number obtained per gram of adipose tissue from BFP at one week of culture was 2-fold higher than in subcutaneous abdominal adipose tissue. Angiogenic marker expression was also higher, and ASC showed multipotent differentiation potential as well. Fifteen min BMP-2 treatment increased ASC cell proliferation and osteogenic differentiation on BCP composed of 60% HA and 40% β-TCP, but not on other scaffolds containing less percentage of HA.
Conclusions: Buccal fat pad is a rich alternative source of ASC suitable for bone tissue engineering. Short stimulation of only 15 minutes with BMP-2 is enough to stimulate ASC proliferation and osteogenic differentiation. Therefore ASC could be treated shortly with BMP-2 and seeded on BCP with 60% HA to improve bone regeneration.
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Ojha, Shalini. "Pericardial fat is a nutritionally regulated depot of brown adipose tissue." Thesis, University of Nottingham, 2015. http://eprints.nottingham.ac.uk/30678/.
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Introduction: Obesity and related cardio-metabolic complications have acquired global epidemic proportions. Suboptimal nutritional environment in early life induces adaptations in energy homeostasis, metabolism and adipose tissue development that may confer short-term survival advantages but are detrimental in later life, particularly if nutrient supply is restored. Brown adipose tissue (BAT) has a unique role in energy homeostasis because it can provide a potential compensatory mechanism against excess weight gain via cold or diet-induced adaptive thermogenesis. Brown adipocytes also have a potential role in lipid and glucose metabolism and BAT activation can increase clearance of lipids and glucose from the circulation. Pericardial fat, particularly epicardial adipose tissue (fat present between the myocardium and the visceral layer of the pericardium), is anatomically and clinically related to cardiac morphology and function and is believed to be a metabolically active organ that affects cardiac function and the evolution of cardiac pathologies. High expression of mRNA for uncoupling protein (UCP) 1 in adult human epicardial adipose tissue suggests that this may be a depot of BAT. Hypotheses: In my thesis, I hypothesised that pericardial adipose tissue is a depot of brown fat in humans and sheep. I also hypothesised that suboptimal nutrition in early life will affect adiposity and development of BAT in this depot. Methods: UCP1 mRNA expression and protein abundance and other BAT and white adipose tissue related genes were studied in pericardial adipose tissue. In the first study, pericardial fat was sampled from newborn and 30 day old sheep born to mothers fed with 100% or 60% of their total metabolisable energy (ME) requirement from 110 day gestation to term. In the second study, pericardial fat was sampled from near-term (140 day gestation) fetuses delivered to mothers fed 100% or 60% of total ME requirement from 28 to 80 days and then fed ad libitum. Gene expression was measured by reverse transcription-polymerase chain reaction and protein abundance by Western blotting and immunohistochemistry. To confirm the presence of BAT in the human epicardial fat depot, relative abundance of UCP1 was measured by Western Blotting in epicardial, paracardial, and subcutaneous fat samples taken from adults. In the final study, epicardial fat samples were collected from 63 children (0-18 years of age) undergoing cardiac surgery and gene expression of UCP1 and other BAT and WAT related genes identified by microarray. The presence of UCP1 was confirmed by immunohistochemistry. Results: Pericardial adipose tissue is a depot of BAT in fetal and newborn sheep. Suboptimal maternal nutrition in late gestation reduces the abundance of UCP1 and downregulates other BAT related genes whilst suboptimal maternal nutrition in early-to-mid gestation followed by ad libitum feeding to term, increases adiposity, enhances UCP1 abundance and upregulates genes involved in brown and white adipogenesis. Epicardial fat from newborn infants, children, adolescents and older adults contains UCP1 confirming that it is a BAT depot in humans. UCP1 gene expression in infancy and early childhood in humans is downregulated in children with poor nutritional states. Conclusions: I have shown that adipose tissue depots present around the heart are a repository of brown fat, at least in humans and sheep. In view of the potential role of BAT in regulation of lipid and glucose metabolism, this may have therapeutic implications for treatment of cardiovascular complications of obesity. Suboptimal nutrition in utero and during early life compromises BAT development. Although the exact mechanism of how these changes affect the propensity towards obesity and metabolic dysregulation remains to be elucidated, a reduction in thermogenesis presents a plausible mechanism for the increased metabolic efficiency associated with nutritional deprivation in early life. BAT persists beyond the neonatal period in to adult life and, therefore, presents a potential target for long lasting nutritional manipulations to promote better health.
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Wiklund, Peder. "Adipose tissue, the skeleton and cardiovascular disease." Doctoral thesis, Umeå universitet, Geriatrik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-42083.
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Cardiovascular disease (CVD) is the leading cause of death in the Western World, although the incidence of myocardial infarction (MI) has declined over the last decades. However, obesity, which is one of the most important risk factors for CVD, is increasingly common. Osteoporosis is also on the rise because of an aging population. Based on considerable overlap in the prevalence of CVD and osteoporosis, a shared etiology has been proposed. Furthermore, the possibility of interplay between the skeleton and adipose tissue has received increasing attention the last few years with the discovery that leptin can influence bone metabolism and that osteocalcin can influence adipose tissue. A main aim of this thesis was to investigate the effects of fat mass distribution and bone mineral density on the risk of MI. Using dual-energy x-ray absorptiometry (DEXA) we measured 592 men and women for regional fat mass in study I. In study II this was expanded to include 3258 men and women. In study III 6872 men and women had their bone mineral density measured in the total hip and femoral neck using DEXA. We found that a fat mass distribution with a higher proportion of abdominal fat mass was associated with both an adverse risk factor profile and an increased risk of MI. In contrast, a higher gynoid fat mass distribution was associated with a more favorable risk factor profile and a decreased risk of MI, highlighting the different properties of abdominal and gynoid fat depots (study I-II). In study III, we investigated the association of bone mineral density and risk factors shared between CVD and osteoporosis, and risk of MI. We found that lower bone mineral density was associated with hypertension, and also tended to be associated to other CVD risk factors. Low bone mineral density was associated with an increased risk of MI in both men and women, apparently independently of the risk factors studied (study III). In study IV, we investigated 50 healthy, young men to determine if a high-impact loading intervention in the form of a series of jumps would lead to changes in glucose and lipid metabolism. We found that the intervention group had significantly lowered serum glucose levels compared to the control group. Changes in all metabolic parameters favored the intervention group with an increase in lipolysis from baseline and a decrease in cholesterol. In summary, the proportion of abdominal and gynoid fat mass displayed contrasting associations to both CVD risk factors and MI risk. Abdominal fat mass was associated with a higher risk while a high proportion of gynoid fat mass was associated with a lower risk. Bone mineral density displayed an inverse association with MI risk, seemingly independently of CVD risk factors, suggesting other explanations to a shared pathogenesis. Finally, high impact loading on the skeleton in young, healthy men decreased serum glucose levels and tended to improve other metabolic parameters, suggesting that the skeleton can affect energy metabolism.
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Axelsson, Jonas. "Fat tissue, adipokines and clinical complications of chronic kidney disease /." Stockholm : Department of Clinical Science, Intervention and Technology, Divisions of Renal Medicine and Baxter Novum, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-653-0/.
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Thapar, Divya. "Osteopontin knockout abates high fat diet-induced insulin resistance and adipose tissue inflammation." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1459910.
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Thesis (M.S.)--University of California, San Diego, 2008.Title from first page of PDF file (viewed January 5, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 43-46).
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Nnodim, J. O. "Morphological studies on the development and the control mechanisms of brown adipose tissue." Thesis, Bucks New University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356211.
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Dziubajlo, Maria. "Factors affecting the composition and physical properties of pig adipose tissue triacylglycerols." Thesis, Imperial College London, 1991. http://hdl.handle.net/10044/1/46754.
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Manolopoulos, Konstantinos. "Adrenergic regulation of regional fat metabolism." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:31dfdca3-e3df-41a6-bf27-74f6ccdcf0a7.
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Introduction: An increased gluteofemoral adipose tissue (AT) mass is associated with a protective cardiovascular and metabolic risk profile, and effective fatty acid retention in femoral AT has been proposed as a possible mechanism. Catecholamines are important regulators of AT lipolysis and blood flow (ATBF). The aim of the thesis was to investigate regional differences in the adrenergic regulation of fatty acid release and ATBF between abdominal and femoral AT in vivo. Furthermore, in vivo regional fatty acid trafficking was studied in a physiological setting over 24 h. Methods: Regional fatty acid trafficking, along with the measurement of ATBF, was studied with the arterio-venous difference technique and stable isotope tracers in healthy volunteers. Adrenergic agonists (isoprenaline, adrenaline) were infused either locally by microinfusion, or systemically. Local microinfusion of adrenoreceptor antagonists (propranolol, phentolamine) was used to characterize specific adrenoreceptor subtype effects. The trafficking of dietary fatty acids was studied over a 24 h period involving three meals containing stable isotope-labelled fatty acids along with intravenous infusions of another labelled fatty acid. Results: Femoral ATBF and lipolysis was less responsive to adrenergic stimulation with adrenaline compared to abdominal AT. This was due to increased femoral α-adrenoreceptor responsiveness. When studied over 24 h, femoral AT showed a lower lipolysis rate compared to abdominal AT, while dietary fatty acids were extracted more avidly by abdominal AT. Uptake of non-dietary fatty acids (derived from very-low-density lipoproteins or unbound non-esterified fatty acids) was comparable between abdominal and femoral AT. Conclusion: There are fundamental differences in response to adrenergic stimuli between abdominal and gluteofemoral tissues and the ability of femoral AT to trap non-dietary fatty acids may provide protection of other tissues from ectopic fatty acid deposition.
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Zieger, Konstanze, Juliane Weiner, Anne Kunath, Martin Gericke, Kerstin Krause, Matthias Kern, Michael Stumvoll, Nora Klöting, Matthias Blüher, and John T. Heiker. "Ablation of kallikrein 7 (KLK7) in adipose tissue ameliorates metabolic consequences of high fat diet-induced obesity by counteracting adipose tissue inflammation in vivo." Springer, 2018. https://ul.qucosa.de/id/qucosa%3A33207.
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Vaspin is an adipokine which improves glucose metabolism and insulin sensitivity in obesity. Kallikrein 7 (KLK7) is the first known protease target inhibited by vaspin and a potential target for the treatment of metabolic disorders. Here, we tested the hypothesis that inhibition of KLK7 in adipose tissue may beneficially affect glucose metabolism and adipose tissue function. Therefore, we have inactivated the Klk7 gene in adipose tissue using conditional gene-targeting strategies in mice. Klk7-deficient mice (ATKlk7 −/−) exhibited less weight gain, predominant expansion of subcutaneous adipose tissue and improved whole body insulin sensitivity under a high fat diet (HFD). ATKlk7 −/− mice displayed higher energy expenditure and food intake, most likely due to altered adipokine secretion including lower circulating leptin. Pro-inflammatory cytokine expression was significantly reduced in combination with an increased percentage of alternatively activated (anti-inflammatory) M2 macrophages in epigonadal adipose tissue of ATKlk7 −/−. Taken together, by attenuating adipose tissue inflammation, altering adipokine secretion and epigonadal adipose tissue expansion, Klk7 deficiency in adipose tissue partially ameliorates the adverse effects of HFD-induced obesity. In summary, we provide first evidence for a previously unrecognized role of KLK7 in adipose tissue with effects on whole body energy expenditure and insulin sensitivity.
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Keuper, Michaela [Verfasser]. "The role of fat cell apoptosis during obesity-associated adipose tissue inflammation / Michaela Keuper." Ulm : Universität Ulm. Fakultät für Naturwissenschaften, 2011. http://d-nb.info/1017543380/34.
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von, Essen Gabriella. "Energy flow and metabolic efficiency attributed to brown adipose tissue." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-140190.
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The large capacity of brown adipose tissue (BAT) to expend energy as heat makes it an interesting potential player in weight regulation and other metabolic conditions. This is of particular interest as it has been recognized that adult humans possess BAT. The protein responsible for the heat production is uncoupling protein 1 (UCP1), which, as the name implies, uncouples the respiratory chain from ATP production; instead heat is produced. Cold is the strongest recruiter and activator of BAT. However, also obesogenic food has a low but nonetheless significant effect on the recruitment and activation of UCP1, although the significance of this has been discussed. In the present thesis, I have studied the effect of diet on BAT and the possibilities for it to be obesity-protective. This can be done by comparing responses in wild-type mice and in UCP1-ablated mice. Since the effect of diet on BAT is low, it is of importance to control the temperature and maintain thermoneutrality. Other confounding factors to keep in mind are differences in actual energy and composition of food and also cohort differences. When controlling all the parameters mentioned and giving the mice the same obesogenic diet, the mice possessing UCP1 compared to UCP1-ablated mice had higher energy expenditure, and lower weight gain, despite eating more. This confirms the presence of a UCP1-dependent diet-induced thermogenesis. Thus, the conclusion must be that possessing UCP1 does result in obesity protection at thermoneutrality. However, the relevance for human energy balance is still not established.At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: Manuscript. Paper 2: Manuscript. Paper 3: Manuscript.
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Meln, Irina [Verfasser], and Ingrid [Akademischer Betreuer] Lohmann. "Conditioning fat for the future: adipose tissue expansion during childhood / Irina Meln ; Betreuer: Ingrid Lohmann." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177383896/34.
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Rodwan, Naima Salem. "Light-Limited Access to Fructose Alters Metabolic Function and Adipose Tissue Catecholaminergic Activity in Mice." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1339615527.
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So, Wing-yan. "Proteome and gene expression analysis in white adipose tissue of diet-induced obese mice." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39367435.
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Werner, Katharina Julia [Verfasser], Lorenz [Gutachter] Meinel, and Torsten [Gutachter] Blunk. "Adipose Tissue Engineering - In vitro Development of a subcutaneous fat layer and a vascularized adipose tissue construct utilizing extracellular matrix structures / Katharina Julia Werner. Gutachter: Lorenz Meinel ; Torsten Blunk." Würzburg : Universität Würzburg, 2014. http://d-nb.info/1111508194/34.
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KUO, HSUAN-CHIH. "Apolipoprotein A-IV Enhances Thermogenesis in Brown Adipose Tissue and Energy Expenditure." Ohio University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1628701770248129.
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So, Wing-yan, and 蘇詠欣. "Proteome and gene expression analysis in white adipose tissue of diet-induced obese mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39367435.
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Kotarsky, Christopher Joseph. "Strategies for the Reduction of Adipose Tissue and Retention of Muscle Mass in Overweight Individuals." Diss., North Dakota State University, 2020. https://hdl.handle.net/10365/32044.
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Purpose: The purpose of this study was to determine whether time-restricted feeding (TRF) was an effective dietary strategy for reducing fat mass and preserving fat-free mass while evaluating potential changes in cardiometabolic biomarkers, hormones, muscle performance, and energy and macronutrient intake after eight weeks of aerobic exercise and resistance training in overweight and obese adults. Methods: This study was a randomized, controlled trial. Sedentary, overweight and obese adults (mean ± SD; age: 44.48 ± 7.28 years; BMI: 29.61 ± 2.62 kg/m2; females: 85.71%; males: 14.29%) were randomly assigned to a TRF or normal feeding (NF) dietary strategy group. The TRF group consumed all calories between 1200 and 2000 hours, whereas the NF group ate their typical diet. All groups completed eight weeks of aerobic exercise and supervised resistance training. Body composition, muscle performance, energy and macronutrient intake, physical activity, and physiological variables were assessed week zero and week nine. Results: A total of 21 participants completed the study (NF: n = 10; TRF: n = 11). A mild energy restriction was seen for the TRF (~300 kcal/day, 14.0%) and NF (~250 kcal/d, 11.0%) groups between baseline and week seven. Losses of total body mass were significantly greater for TRF (3.3%) relative to NF (0.2%), of which TRF had significantly greater losses of fat mass (9.0%) compared to NF (3.3%) despite similar reductions in energy intake. Lean mass increased across the intervention for both TRF (0.6%) and NF (1.9%), with no group differences. Conclusion: These data support the use of TRF and concurrent exercise training as a short-term dietary strategy for reducing fat mass and preserving lean mass in overweight and obese adults.
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Kreier, Felix. "Autonomic nervous control of white adipose tissue studies on the role of the brain in body fat distribution /." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2005. http://dare.uva.nl/document/77915.
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Ronkainen, J. (Justiina). "Role of Fto in the gene and microRNA expression of mouse adipose tissues in response to high-fat diet." Doctoral thesis, Oulun yliopisto, 2016. http://urn.fi/urn:isbn:9789526213453.
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Abstract Obesity is associated with greater risk of several diseases, such as type 2 diabetes and metabolic syndrome. Single nucleotide polymorphisms (SNP) within the fat mass- and obesity-associated gene FTO are robustly associated with increased body mass index (BMI) in several age and ethnic groups. Studies with transgenic mice support a mechanistic role for FTO protein in energy metabolism. Fto-deficient mice are leaner than wild-type and overexpression of Fto leads to obese phenotype; however, the precise mechanism of FTO action in the control of BMI has remained obscure. Fto mRNA is most abundant in the brain while high expression is present also in white and brown adipose tissues (WAT and BAT, respectively). WAT stores the nutritional energy and BAT dissipates it to produce heat. Furthermore, these organs participate in a complex endocrine network affecting the whole body metabolism, which is more or less disrupted in obesity. In the browning process, white adipocytes begin to manifest brown characteristics. MicroRNAs (miRNA) are small RNA molecules, which fine-tune post-transcriptionally the expression of genes important in several cellular processes, including WAT and BAT differentiation and browning of WAT. FTO has been shown to participate in these processes as well as miRNA regulation. The current study used a new Fto-deficient mouse model to reveal deeper insights into the role of Fto on genes affecting WAT and BAT differentiation and function, as well as WAT browning. Furthermore, the effects of Fto on the miRNA regulation in WAT browning and BAT were investigated. Our results supported a role for Fto in adipose tissue. Fto-deficient mice were resistant to diet-induced obesity and their WAT and BAT adipocytes did not become hypertrophic similar to wild-type on high-fat diet. Furthermore, the expression of genes affecting adipose tissue differentiation and function was altered in Fto-deficient WAT and BAT, especially after high-fat diet, and the changes may be mediated via altered miRNA expression. Fto-deficient WAT was more susceptible to browning, which in part contributed to the lean phenotype of these mice. Current study supported a role for Fto in whole body metabolism and adaptation of adipose tissue to changes in dietary environmentTiivistelmä Lihavuus on toistuvasti yhdistetty useisiin liitännäissairauksiin, kuten tyypin 2 diabetekseen ja metaboliseen oireyhtymään. FTO-geenissä (fat mass- and obesity-associated) esiintyvien yhden nukleotidin muutoksien (single nucleotide polymorphia, SNP) on useissa ikä- ja etnisissä ryhmissä raportoitu liittyvän korkeampaan painoindeksiin ihmisillä. Muuntogeenisillä hiirillä tehdyt tutkimukset tukevat FTO:n mekanistista roolia energia-aineenvaihdunnassa, sillä Fto-poistogeeniset hiiret ovat villityypin hiiriä laihempia ja sen yliekspressio johtaa ylipainoon. FTO:n tarkka rooli painon säätelyssä on kuitenkin vielä epäselvä. Fto:ta tuotetaan eniten aivoissa, mutta myös valkoisessa ja ruskeassa rasvassa. Valkoinen rasva varastoi ravinnosta saatavan energian ja ruskea hajottaa sitä lämmöntuotantoon. Näillä kudoksilla on lisäksi tärkeä rooli energia-aineenvaihdunnan monimutkaisessa verkostossa. Valkoisen rasvakudoksen ruskettumisprosessissa valkoiset rasvasolut alkavat muistuttaa ruskeita rasvasoluja. Mikro-RNA:t (miRNA) ovat pieniä RNA-juosteita, jotka hienosäätävät geenien ekspressiota transkription jälkeen ja vaikuttavat useisiin solun tärkeisiin tapahtumiin, myös valkoisen ja ruskean rasvasolun erilaistumiseen ja ruskettumiseen. FTO osallistuu näihin prosesseihin sekä miRNA-säätelyyn. Tämän tutkimuksen tavoitteena oli selventää Fto:n roolia valkoisen ja ruskean rasvakudoksen erilaistumisessa ja toiminnassa Fto-poistogeenisen hiirimallin avulla. Lisäksi selvitettiin Fto:n vaikutuksia valkoisen rasvan ruskettumiseen ja ruskean rasvan toimintaan osallistuvien miRNA:iden säätelyyn. Tulokset tukivat FTO:n roolia rasvakudoksessa. Fto-poistogeeniset hiiret eivät lihoneet rasvaisella ruokavaliolla eivätkä niiden rasvasolut varastoineet rasvaa yhtä paljon kuin villityypin hiirillä rasvaisen ruokavalion jälkeen. Lisäksi Fto-poistogeenisen rasvakudoksen erilaistumiseen ja toimintaan liittyvien geenien esiintyvyys muuttui erityisesti rasvaisella ruokavaliolla. Nämä muutokset voivat osittain selittyä muuttuneella miRNA-säätelyllä. Tulokset viittasivat siihen, että Fto-poistogeeninen valkoinen rasvakudos oli alttiimpaa ruskettumiselle, mikä osaltaan vaikutti Fto-poistogeenisten hiirten laihuuteen. Tutkimus tuki Fto-geenin roolia energia-aineenvaihdunnan säätelyssä sekä rasvakudoksen mukautumisessa ruokavalion muutoksiin
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Ntinas, Petros. "Function and activation of human adipose tissue : the role of genes in the link between physical activity and brown adipose-like phenotype." Thesis, University of Wolverhampton, 2017. http://hdl.handle.net/2436/620509.
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Background: Excess white adipose tissue (WAT) in humans is considered as a harmful health index. However, increased brown adipose tissue (BAT) and brown-like adipose tissue activity are associated with increased resting energy expenditure (REE) that may help to control body weight. Exercise may enhance browning formation of WAT and reduce WAT that may lead to health improvements. Aims: a) to examine the effects of physical activity on the link between peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1α) and fibronectin type III domaincontaining protein 5 (FNDC5) genes in muscle, circulating Irisin and uncoupling protein one (UCP1) of WAT in humans (study 1); b) to examine the relationship between UCP1 mRNA and protein expression as well as PGC-1α, peroxisome proliferatoractivated receptor alpha (PPARα) and PPARγ genes with physical activity levels in WAT of healthy men (study 2); c) to examine the effects of different types of exercise and de-training on the UCP1 mRNA and protein expression (study 3), and d) on leptin mRNA in WAT of healthy men (study 4). Method: Study 1: A systematic review was conducted using the Preferred Reporting Items for Systematic Reviews and Meta- Analyses. Studies 2-4: The total of 46 healthy men subjected to measurements for physical activity levels, diet, anthropometry, body composition, REE, peak oxygen consumption, 1-repetition maximum and provided subcutaneous fat biopsies to determine mRNA and protein expression of six genes in one cross-sectional study and one randomized controlled trial. Results: Study 1: No link was found between PGC- 1α and FNDC5, circulating Irisin and UCP1 of WAT in response to physical activity. Study 2: The mRNA of, UCP1, PGC-1α, PPARα and PPARγ genes of WAT were not associated with physical activity levels. The UCP1 protein expression however, was negatively associated with physical activity levels. Studies 3-4: Different types of chronic exercise and de-training do not affect UCP1 mRNA and protein expression 3 and leptin mRNA in WAT. However, effect size analyses demonstrated increased UCP1 mRNA and protein expression, PPARγ and leptin in response to chronic exercise. Conclusions: There is no evidence to support the link between PGC-1α and FNDC5 in human muscle or the link between FNDC5 and circulating Irisin and UCP1 in WAT in response to exercise. There are no effects of exercise and de-training on browning formation of WAT and no link between browning formation indices and REE, body weight as well as leptin mRNA in healthy men. Further research is required to elaborate the aforementioned phenomena.
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Olhager, Elisabeth. "Studies on adipose tissue, body fat, body water and energy expenditure during the first four months of infancy using magnetic resonance imaging, skinfold measurements and the doubly labelled water method /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med798s.pdf.
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Chiasson, Martine. "Influence of Menarche on Body Weight. A Systematic Review and Meta-Analysis." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31700.
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It has been shown that post-menarcheal girls are more likely to have increased their body weight and body mass index (BMI) than pre-menarcheal girls of the same age. In addition to the metabolic changes which occur during this interval, behavioural risk factors synergize to promote weight gain, putting adolescents at a much higher risk for excess weight gain and its associated health complications. Moreover, obesity during adolescence increase the risk of becoming an obese adult. A systematic review of English and French articles using MEDLINE, EMBASE, Cochrane, and CINAHL was conducted. Studies underwent a three level screening assessment by two independent assessors. Only studies with post-menarcheal weight change information were selected for data extraction and quality assessment, which was conducted by two independent reviewers. A meta-analysis was conducted for weight change and included 389 girls. Five studies discussed the effects of menarche on body weight change. Pooled results for three studies indicated a 10.39 kg increase from pre to post-menarche (95% CI, 9.16-11.62). The other two studies showed significant increases in body fat mass (p<0.05) and higher skinfolds measurements for post-menarcheal girls compared to pre-menarcheal girls. It is important to further explore the bio-psychosocial and environmental factors influencing the weight, especially the total fat mass and body fat distributions in young adolescent girls during the menarche transition in order to develop and evaluate preventive intervention strategies to prevent adolescent and adult obesity.
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Li, Xiaofeng [Verfasser]. "Activation of CXCR7 improves hyperlipidemia by increasing cholesterol storage in adipose tissue and limits atherosclerosis / Xiaofeng Li." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2013. http://d-nb.info/104665036X/34.
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Westcott, Edward Daniel Anders. "Abnormalities of lipid storage in perinodal adipose tissue and their implications for the development of Crohn's disease." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516971.
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Menon, Vinal. "The contribution of visceral fat to positive insulin signaling in Ames dwarf mice." Master's thesis, University of Central Florida, 2013. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/5818.
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Ames dwarf (df/df) mice are homozygous for a spontaneous mutation in the prop1 gene due to which there is no development of anterior pituitary cells – somatotrophs, lactotrophs and thyrotrophs, leading to a deficiency of growth hormone (GH), prolactin (PRL) and thyrotropin (TSH). They tend to become obese as they age, but still live longer and healthier lives compared to their wild-type littermates, being very insulin sensitive, showing no signs of diabetes and cancer. These mutant mice also have high circulating levels of anti-inflammatory and anti-diabetic adiponectin. Plasma levels of this adipokine usually decrease with an increase in accumulation of visceral fat (VF). We thus believe that VF in df/df mice, developed in the absence of GH signaling, may be functionally different from the same fat depots in normal (N) mice and may be beneficial, rather than detrimental, to the overall health of the animal. We performed surgeries involving removal of VF depots (epididymal and perirenal fat) in both groups of mice and hypothesize that the beneficial effects of visceral fat removal (VFR) will be present exclusively in N mice as VF in df/df mice contributes to enhanced insulin sensitivity by producing decreased levels of pro-inflammatory adipokines like TNF? and IL-6. We found that VFR improved insulin sensitivity only in N mice but not in the df/df mice. This intervention led to an upregulation of certain players of the insulin signaling pathway in the skeletal muscle of N mice only, with no alteration in df/df mice. The subcutaneous fat of df/df mice showed a downregulation of these insulin signaling genes upon VFR. Compared to N mice, epididymal fat of df/df mice (sham-operated) had increased gene expression of some of the players involved in insulin signaling and a decrease in transcript levels of TNFa. Ames dwarf mice had decreased levels of IL-6 protein in EF and in circulation. High circulating levels of adiponectin and decreased levels of IL-6 in circulation could contribute to the high insulin sensitivity observed in the Ames dwarf mice. Understanding the mechanisms responsible for VF having positive effects on insulin signaling in df/df mice would be important for future treatment of obese diabetic patients.M.S.
Masters
Molecular Biology and Microbiology
Medicine
Biotechnology
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Berg, Frida. "Genetic Analysis of Fat Metabolism in Domestic Pigs and their Wild Ancestor." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7089.
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Amdi, Charlotte. "The effect of varying feeding levels for thin and fat sows during gestation on muscle and adipose tissue of progeny." Thesis, Royal Veterinary College (University of London), 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572440.
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Paglialunga, Sabina. "Regulation of fatty acid storage and utilization: the role of Acylation Stimulating Protein, an anabolic adipose tissue hormone." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66839.
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Adipose tissue is an important contributor to energy homeostasis and the discovery that adipose tissue produces a number of hormones involved in regulating energy storage and energy utilization has been a topical area of research. Acylation stimulating protein (ASP/C3adesArg) is an adipose tissue derived hormone that stimulates fatty acid uptake and storage in adipocytes. ASP stimulates triglyceride (TG) synthesis via its receptor, C5L2. C5L2 also binds C5a, an anaphylactic protein structurally similar to ASP, yet its function as an active receptor for C5a is still under debate. However, in adipocytes ASP affects TG synthesis via increased diacylglycerol acyltransferase activity, glucose transport and indirect stimulation of lipoprotein lipase (LPL) activity. LPL is often referred to as a 'gatekeeper of postprandial TG' and subjects with a genetic mutation in LPL suffer from hyperchylomicronemia (excess dietary lipids). The overall objective of this thesis was to examine the role of ASP in lipid metabolism by tracking fatty acid fluxes in human subjects and animal models. This was investigated by 1) evaluating the fasting and postprandial plasma ASP levels in subjects deficient in LPL and 2) determining the consequences of fatty acid repartitioning with respect to adipose tissue storage and muscle utilization. The latter examined fatty acid storage and oxidation in two mouse models, ASP-deficient C3 knockout (KO) and ASP receptor-deficient C5L2 KO mice. Novel findings showed that both homozygote and heterozygote carriers of an LPL mutation displayed elevated fasting ASP levels, possibly due to the accumulation of chylomicrons in these subjects, since fibrate treatment which reduces TG levels also decreased ASP levels in LPL heterozygotes. In addition, this thesis showed that both C3KO and C5L2 KO mice displayed altered adipocyte morphology, reduced adipose tissue TG synthesis capacity and increased skeleLe tissu adipeux est un régulateur important de l'homéostasie énergétique de l'organisme. Outre sa fonction de réserve énergétique, le tissu adipeux est capable de produire une grande variété d'hormones. Celles-ci jouent de nombreux rôles dans le contrôle du stockage et l'utilisation de l'énergie et la compréhension de leurs fonctions est un sujet de pointe en recherche. La protéine stimulant l'acylation (ASP/C3adesArg) est une hormone dérivée du tissu adipeux qui stimule le captage et le stockage des acides gras (AG) chez les adipocytes. L'ASP stimule également la synthèse des triglycérides (TG) via son récepteur, le C5L2. Le C5L2 est aussi reconnu comme pouvant lier le C5a, une protéine anaphylactique similaire à l'ASP, mais son activation suite à cette liaison reste controversée. Pour sa part, l'ASP agit sur la synthèse des TG via un accroissement de l'activité de la diacylglycérol acyltransférase chez les adipocytes. L'ASP augmente aussi le transport du glucose et stimule indirectement l'activité de la lipoprotéine lipase (LPL). La LPL est reconnue comme étant capable de contrôler les niveaux de TG postprandiaux. Les personnes qui possèdent une mutation dans le gène de la LPL souffrent d'hyperchylomicronémie (un excès de lipides alimentaires). L'objectif principal de cette thèse était de déterminer le rôle de l'ASP dans le métabolisme lipidique en évaluant les fluctuations des AG tant chez l'humain que chez l'animal. Cet objectif a été réalisé en : 1) évaluant les niveaux d'ASP à jeun et postprandiaux chez des personnes déficientes en LPL, en 2) regardant les conséquences d'un changement dans la répartition des AG en relation avec le stockage dans le tissu adipeux et l'utilisation par le muscle et finalement en 3) examinant le stockage et l'oxydation des AG chez deux modèles murins; soient des souris déficientes en protéine C3 (ASP déficiente obl
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Behrman, Roger L. "The effects of dietary fat and age on adipose tissue composition and fatty acid synthesis levels in strain A/ST mice." Virtual Press, 1990. http://liblink.bsu.edu/uhtbin/catkey/722436.
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Differences in fatty acid distributions in adipose tissue and fatty acid synthetase levels in the liver were determined in Strain A/ST mice of different ages and diets. Since fatty acids have been found to be influential in many disease processes such as heart disease and cancer, which become more prevalent with increasing age, it is important to understand the processes of fat metabolism and changes that occur during the life-stage of senescence. Fatty acid distributions were determined by gas liquid chromatography and fatty acid synthetase (FAS) activities by spectrophotometry.The data from FAS analyses indicated that the mice fed the highfat palmitic acid and low-fat corn oil diets were similar to previous research. The mice fed the stearic acid diets had FAS activity that was affected in a very different manner than other high-fat diets.The results of this study also indicated that aging does not significantly effect the distribution of fatty acids in the adipose tissue of experimental mice. Weight gain in the middle age mice appears to be the result of an increase in all types of fatty acids and not just increased storage of one or a few types.Department of Biology
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Lindstrom, Rachel C. "Fat mass defense in humans: Cellular and molecular mechanisms underlying adipose tissue accumulation over time and following suction lipectomy in humans." Connect to online resource, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3337123.
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Kotzé-Hörstmann, Liske. "Effects of adipose tissue extracellular matrix components on body fat distribution and insulin sensitivity in black and white South African women." Doctoral thesis, Faculty of Health Sciences, 2018. http://hdl.handle.net/11427/30585.
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The global burden of non-communicable diseases (NCD’s) is unacceptably high and disproportionately affects developing countries such as South Africa (SA). Black SA women have a higher prevalence of obesity and a greater associated risk for developing metabolic diseases (such as type 2 diabetes mellitus) than their white counterparts. An improved understanding of the ethnic-specific mechanisms underlying the increased risk of T2DM in black SA women is needed to inform future studies aimed at reducing the prevalence of this diseases.
One of the major determinants of insulin resistance is android/central body fat partitioning, with visceral adipose tissue (VAT) enlargement, in particular, being closely associated with increased risk. Conversely, lower-body fat accumulation is considered to be protective. However, these relationships between body fat distribution and its metabolic effects are altered by ethnicity. Black SA women have less abdominal and greater gluteal-femoral subcutaneous adipose tissue (SAT) but are more insulin resistant compared to BMI- and waist circumference-matched white SA women. A similar profile has been described in black African-American women.
The reduced protective effect of peripheral fat distribution in black women remains to be understood. The primary aim of this thesis was positioned within the context of adipose tissue expandability hypothesis, and aimed to examine the hypothesis that differences in SAT extracellular matrix (ECM)- and hypoxia-related gene expression and their ethnic specific associations with body composition and insulin sensitivity may explain, in part, the higher rates of insulin resistance in black compared to white South African women.
Therefore, it was hypothesized that, as a consequence of increased adipose tissue hypertrophy in the gluteal depot of obese black compared to obese white women, gluteal SAT adipose tissue hypoxia and ECM component gene expression is higher in black compared to white women, and associates with their reduced insulin sensitivity (SI) and higher insulin response. In order to address this hypothesis, four research studies were designed.
The first study (Chapter 3) in this thesis aimed to compare depot-specific (abdominal vs. gluteal) expression of hypoxia and ECM genes in normal-weight and obese black and white women, and to examine the ethnic-specific associations between these genes and body composition, measures of insulin sensitivity and secretion and inflammatory gene expression in black and white SA women by using a gene expression (Reverse transcription polymerase chain reaction (RT-PCR)) analysis.
This thesis showed for the first time that hypoxia inducible factor 1 (HIF-1α), collagen type V α1 (Col5A1) and type VI α1 (COL6A1) gene expression were higher in the gluteal, but not the abdominal SAT depots, of black compared to white women, and associated with reduced insulin sensitivity in black women only. The expression of the hypoxia and ECM genes associated with inflammatory gene expression in both the gluteal and abdominal SAT depots of black women, whereas the expression of these genes associated with the inflammatory gene expression mostly in the abdominal SAT depots of white women.
The second study (Chapter 4) tests the hypothesis that higher hypoxia and ECM related gene expression would associate with higher central fat mass accumulation in black women and that the expression of these genes may be associated with changes in the measures of insulin sensitivity in black and white women. Thus, this longitudinal study aimed to determine whether changes in body composition and insulin sensitivity variables over a 5 year follow-up period associated with variations in hypoxia and ECM related gene expression in the gluteal SAT of black and white women. Over the 5-year follow-up period, increased body fat mass in white women associated with increased PPARγ mRNA expression whereas increased body fat mass in black women associated with lower COL5A1 expression. Furthermore, HIF-1α, and COL6A1 expression correlated positively with the change in fasting insulin concentrations in black but not in white women.
It is not clear whether high circulating insulin may directly increase HIF-1α expression and contribute to the formation of excess ECM, or whether increased insulin may simply be a concomitant downstream effect of increased insulin resistance, as a consequence of increased fibrosis and the generation of inflammation. By using a cell culture based study, the third study in this thesis (chapter 5), investigated the effects of increasing insulin concentrations on the expression of hypoxia and ECM related genes under normoxic and hypoxic conditions in mature 3T3-L1 adipocytes. It was found that insulin and hypoxia treatment significantly elevated HIF-1α mRNA and protein levels but that the observed effects were not additive. Further, hypoxia, but not insulin treatment, increased the expression of Col5a1 and Col6a1 protein but not mRNA levels in mature 3T3-L1 adipocytes.
By using a genotyping analysis, the fourth study (Chapter 6) aimed to determine whether variants within two ECM component gene polymorphisms, collagen type 5α1 (COL5A1) rs12722 (C/T) and type 6α1 (COL6A1) rs35796750 (C/T) associates with body fat distribution and insulin resistance in black and white women. Allele and genotype distributions of the COL5A1 rs12722 and COL6A1 rs35796750 polymorphisms, as well as body fat distribution were significantly different between black and white women, the T- variant of the COL5A1 rs12722 polymorphism was associated with significantly less central fat mass, characterised by a smaller waist circumference and lower VAT, and this effect was independent of ethnicity. In addition, T- variant of the COL5A1 rs12722 polymorphism was associated with lower fasted insulin concentrations and HOMA-IR in white but not in black women. In contrast, no genotype associations between COL6A1 rs35796750 and any of the body fat mass, its distribution and insulin resistance measures in black or white women were reported.
This thesis used a hypothesis driven approach to provide preliminary evidence that the gluteal depot of obese black women has higher expression of hypoxia and ECM genes compared to that of obese white women and provides novel insight into the apparent paradox of reduced insulin sensitivity despite lower VAT and greater peripheral SAT accumulation in black compared to white women. An improved understanding of the ethnic-specific mechanisms underlying the increased risk of T2DM in black SA women will enable the development of cost-effective preventative care strategies within the South African demographic
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Lundgren, Magdalena. "Interplay between hormones, nutrients and adipose depots in the regulation of insulin sensitivity : an experimental study in rat and human adipocytes." Doctoral thesis, Umeå : Public Health and Clinical Medicine, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-677.
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Mahat, Bimit. "The Effects of Hypoxia on Human Adipose Tissue Lipid Storage and Mobilization Functions: From Primary Cell Culture to Healthy Men." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36865.
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Adipose tissue plays a central role in the regulation of lipid storage and mobilization. A tight control between adipose tissue lipid storage and mobilization functions must be exerted to prevent an overload of lipids at other organs such as the heart, liver and skeletal muscles, and favor the risk of developing metabolic disorders, such as Type 2 diabetes and cardiovascular diseases (CVD). There is strong evidence from animal studies that low oxygen levels (hypoxia) are noted in adipose tissue as the mass of the organ excessively expands and, in turn, exacerbates some adipose tissue functions. Whether hypoxia exposure, which could be derived from reduced environmental oxygen availability, disease or a combination of both, affects adipose tissue lipid storage and mobilization functions in humans is not well known. Using in vitro and in vivo approaches, this thesis aimed at characterizing the effects of hypoxia on human adipose tissue lipid storage and lipid mobilization functions. Study I investigated how hypoxia can modulate human adipose functions such as lipid storage and lipid mobilization in vitro. Study II examined whether acute intermittent hypoxia, which simulates obstructive sleep apnea, affects adipose tissue lipid storage/mobilization functions and triglyceride levels in healthy young men in postprandial state. Study III tested the effect of an acute 6-hour continuous exposure to hypoxia (fraction of inspired oxygen (FIO2) = 0.12)) on plasma triglyceride levels in healthy young men in the fasting state. Study I indicates that both acute (24h) and chronic (14d) hypoxia (3%, and 10% O2) modulate human adipose tissue lipid storage and mobilization functions in a different manner. Study II demonstrates that acute exposure to intermittent hypoxia (6h) is sufficient to increase plasma non-esterified fatty acids (NEFA) levels, as well as insulin levels, but does not alter circulating triglyceride or subcutaneous adipose tissue lipid storage and/or mobilization capacity ex vivo in healthy men. Study III shows that acute exposure to normobaric hypoxia increases circulating NEFA and glycerol concentrations but did not translate in altering circulating triglycerides in fasting healthy men. In conclusion, our observations suggest that an exposure to reduced oxygen levels impairs human adipose tissue storage and/or mobilization functions, a phenomenon known in the development of metabolic disorders, such as Type 2 diabetes and CVD.
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Rockstroh, Denise, Kathrin Landgraf, Isabel Viola Wagner, Julia Gesing, Roy Tauscher, Nicole Lakowa, Wieland Kiess, et al. "Direct evidence of brown adipocytes in different fat depots in children." Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-161428.
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Recent studies suggested the persistence of brown adipocytes in adult humans, as opposed to being exclusively present in infancy. In this study, we investigated the presence of brown-like adipocytes in adipose tissue (AT) samples of children and adolescents aged 0 to
18 years and evaluated the association with age, location, and obesity. For this, we analysed AT samples from 131 children and 23 adults by histological, immunohistochemical and expression analyses. We detected brown-like and UCP1 positive adipocytes in 10.3% of 87 lean children (aged 0.3 to 10.7 years) and in one overweight infant, whereas we did not find brown adipocytes in obese children or adults. In our samples, the brown-like adipocytes were interspersed within white AT of perirenal, visceral and also subcutaneous depots. Samples with brown-like adipocytes showed an increased expression of UCP1
(>200fold), PRDM16 (2.8fold), PGC1α and CIDEA while other brown/beige selective markers, such as PAT2, P2RX5, ZIC1, LHX8, TMEM26, HOXC9 and TBX1 were not significantly different between UCP1 positive and negative samples. We identified a positive correlation
between UCP1 and PRDM16 within UCP1 positive samples, but not with any other brown/beige marker. In addition, we observed significantly increased PRDM16 and PAT2 expression in subcutaneous and visceral AT samples with high UCP1 expression in adults. Our data indicate that brown-like adipocytes are present well beyond infancy in subcutaneous
depots of non-obese children. The presence was not restricted to typical perirenal locations, but they were also interspersed within WAT of visceral and subcutaneous depots.
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Negri, Irene. "P2Y2 nucleotide receptor is a regulator of cardiac adipose tissue and its fat-associated lymphoid clusters at basal state and after myocardial infarction." Doctoral thesis, Universite Libre de Bruxelles, 2020. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/312212.
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The research of new therapeutic strategies for cardiovascular diseases has seen in the last 15 years the introduction of a new participant: pericardial adipose tissue (PAT). This tissue is able to modulate cardiac function and its volume was sometimes linked to risk of cardiovascular diseases. Moreover, adipose-derived stem cells (ASCs) isolated from PAT are considered as the best suitable for new regenerative strategies aiming at healing ischemic myocardium. Although the interests in understanding the functions and the formation of pericardial adipose tissue are high, the current knowledge on this tissue is still scarce. In this work, the starting point was the consideration that nucleotide receptors are established regulators of many biological functions, including the differentiation of adult mesenchymal stem cells, immunity and inflammatory process. The P2Y4 receptor has been recently recognized as a negative regulator of cardiac fat formation and ASCs differentiation. The purpose of this thesis was to analyze the involvement of the nucleotide receptor P2Y2 in the formation of pericardial adipose tissue (PAT) and its ASCs differentiation. We also investigated the possible contribution of this receptor to the functions of recently discovered fat-associated lymphoid clusters (FALCs). Our study analyzed the PAT of mice deficient for P2Y2 at basal conditions and in a model of myocardial infarction. P2Y2-null mice showed a lower mass of PAT compared to WT, which was correlated with decreased adipogenic differentiation and maturation potential of pericardial ASCs in vitro. PAT of basal P2Y2-deficient mice displayed a reduced density of FALCs due to a reduced number of B cells. RNA-sequencing experiments identified many P2Y2 target genes in PAT linked to immunomodulation. We identified a polarization of FALCs macrophages towards anti-inflammatory M2c subtype in P2Y2-null mice. We correlated it with a decreased number of follicular helper T cells, known to contribute to B cell expansion in germinal centers. These data could be correlated with increased apoptosis of B lymphocytes. The data obtained using the mouse infarct model confirmed an expected enlargement of pericardial FALCs in ischemic conditions. P2Y2-null mice were characterized by a reduced expansion of B cells and myeloid cells migration in PAT. These results suggested a participation of P2Y2 receptor in regulating the post-MI inflammatory response by modulating the leukocytes populations in the pericardial adipose tissue’s lymphoid clusters. The effect of P2Y2 on PAT post-ischemic inflammatory state could contribute to the P2Y2-mediated cardioprotective effect of UTP described in previous literature. Our study defines P2Y2 nucleotide receptor as a regulator of the formation of pericardial fat and its inflammatory status in ischemic conditions. P2Y2 receptor could represent an interesting therapeutic target for the regulation of PAT functions before and after MI. In general, a better comprehension of PAT and its consideration in the post-ischemic regeneration process could lead to the development of new therapeutic strategies for treating cardiovascular diseases and the adjustment of existing therapies.Durant les 15 dernières années, un nouvel arrivant a fait son apparition dans la recherche de nouvelles approches thérapeutiques dans le domaine cardiovasculaire: le tissu adipeux cardiaque. Ce tissu est capable de moduler les fonctions cardiaques et son volume a pu être associé parfois à un risque de maladie cardiovasculaire. De plus, les cellules souches dérivées du tissu adipeux (ASCs) cardiaque sont considérées comme les mieux appropriées pour des stratégies thérapeutiques visant la réparation du myocarde ischémié. Bien que la compréhension de la fonction et de la formation du tissu adipeux cardiaque présente un intérêt majeur, la connaissance actuelle de ce tissu particulier est encore assez limitée. Pour le présent travail, le point de départ a été l’observation que les récepteurs nucléotidiques sont des régulateurs établis de nombreuses fonctions biologiques, incluant la différentiation des cellules souches mésenchymateuses et plus généralement la régulation de la réponse immune et inflammatoire. Le récepteur P2Y4 a été récemment reconnu comme un régulateur négatif de la formation du tissu adipeux cardiaque et de la différentiation des ASCs. Le but de cette thèse a été l’étude de l’implication du récepteur nucléotidiques P2Y2 dans la formation du tissu adipeux péricardique (TAP) et la différentiation des ASCs. Nous avons également investigué la contribution possible de ce récepteur dans la fonction des structures leucocytaires associées au tissu adipeux appelées FALCS pour fat-associated lymphoid clusters.Nous avons étudié le TAP de souris déficientes pour le récepteur P2Y2 à l’état de base et dans un modèle d’infarctus du myocarde. Les souris P2Y2 knock-out (KO) présentent une masse réduite du TAP corrélée avec le fait que l’absence du P2Y2 diminue la différentiation adipogénique et le potentiel de maturation des ASCs péricardiques in vitro. Le PAT des souris P2Y2 KO présentent une diminution de la densité de FALCs à l’état de base, principalement due à un nombre réduit de lymphocytes B, potentiellement corrélé à une apoptose accrue observée dans ces cellules. Nos expériences de RNA-sequencing ont identifié de nombreux gènes cibles du P2Y2 dans le PAT impliqués dans l’immunomodulation. Nous avons identifié une polarisation des macrophages de type M2c dans les FALCs de souris P2Y2 KO. Nous l’avons corrélée avec une diminution des lymphocytes T helper folliculaires connus pour contribuer à l’expansion des lymphocytes B dans les centres germinaux. Les données obtenues dans le modèle d’infarctus chez la souris ont confirmé une augmentation des FALCs péricardiques dans les conditions d’ischémie cardiaque. Les souris P2Y2 KO sont caractérisées par une expansion réduite des lymphocytes B et des cellules myéloïdes dans le TAP. Ces résultats suggèrent une participation du récepteur P2Y2 dans la régulation de la réponse inflammatoire post-infarctus par la modulation des populations leucocytaires dans les clusters lymphocytaires du tissu adipeux cardiaque. L’effet du P2Y2 sur l’état inflammatoire post-ischémique pourrait contribuer à l’effet cardioprotecteur de l’UTP médié par le P2Y2 et précédemment décrit dans la littérature.Notre étude définit le récepteur nucléotidique P2Y2 comme un régulateur de la formation du tissu adipeux péricardique et de son niveau inflammatoire dans des conditions ischémiques. Le récepteur P2Y2 pourrait représenter une cible thérapeutique intéressante pour la régulation des fonctions du PAT avant et après infarctus du myocarde. Plus généralement, une meilleure compréhension du tissu adipeux cardiaque et de son implication dans le processus de régénération cardiaque pourrait mener au développement de nouvelles stratégies thérapeutiques dans le traitement de maladies cardiovasculaires et à l’ajustement de thérapies déjà existantes.
Doctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
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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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Spence, Jeremiah E. "The Effects of Testicular Nerve Transection and Epididymal White Adipose Tissue Lipectomy on Spermatogenesis in Syrian Hamster." Digital Archive @ GSU, 2008. http://digitalarchive.gsu.edu/biology_theses/17.
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Previous investigators demonstrated that epididymal white adipose tissue (EWAT) lipectomy suppressed spermatogenesis and caused atrophy of the seminiferous tubules. EWAT lipectomy, however, may disrupt testicular innervation, which reportedly compromises testicular function. To resolve this confound and better clarify the role of EWAT in spermatogenesis, three experimental groups of hamsters were created in which: i.) the superior and inferior spermatic nerves were transected (SSNx) at the testicular level, ii.) EWAT was extirpated (EWATx), and iii.) testicular nerves and EWAT were left intact (SHAM controls). It was hypothesized that transection of the superior and inferior spermatic nerves would disrupt normal spermatogenesis. The findings indicate a significant reduction in spermatogenic activity and marked seminal tubule atrophy within the EWATx testis, as compared to the SSNx and controls testes, which did not differ significantly from each other. From these data, it is concluded that EWAT, and not testicular innervation, is central to normal spermatogenesis.
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Hübers, Mark [Verfasser]. "Associations between anthropometric traits, detailed body composition, fat fraction per adipose tissue and cardiometabolic risks: differences between children, adolescents and adults / Mark Hübers." Kiel : Universitätsbibliothek Kiel, 2018. http://d-nb.info/115859755X/34.
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Hung, Chien-Min. "mTORC2 Promotes Lipid Storage and Suppresses Thermogenesis in Brown Adipose Tissue in Part Through AKT-Independent Regulation of FoxO1: A Dissertation." eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/845.
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Recent studies suggest adipose tissue plays a critical role in regulating whole body energy homeostasis in both animals and humans. In particular, activating brown adipose tissue (BAT) activity is now appreciated as a potential therapeutic strategy against obesity and metabolic disease. However, the signaling circuits that coordinate nutrient uptake and BAT function are poorly understood. Here, I investigated the role of the nutrient-sensing mTOR signaling pathway in BAT by conditionally deleting Rictor, which encodes an essential component of mTOR Complex 2 (mTORC2) either in brown adipocyte precursors or mature brown adipocytes. In general, inhibiting BAT mTORC2 reduces glucose uptake and de novo lipogenesis pathways while increases lipid uptake and oxidation pathways indicating a switch in fuel utilization. Moreover, several key thermogenic factors (Ucp1, Pgc1α, and Irf4) are elevated in Rictor-deficient BAT, resulting in enhanced thermogenesis. Accordingly, mice with mTORC2 loss in BAT are protected from HFD-induced obesity and metabolic disease at thermoneutrality. In vitro culture experiments further suggest that mTORC2 cell-autonomously regulates the BAT thermogenic program, especially Ucp1 expression, which depends on FoxO1 activity. Mechanistically, mTORC2 appears to inhibit FoxO1 by facilitating its lysine-acetylation but not through the canonical AKT-mediated phosphorylation pathway. Finally, I also provide evidence that β-adrenergic signaling which normally triggers thermogenesis also induces FoxO1 deacetylation in BAT. Based on these data, I propose a model in which mTORC2 functions in BAT as a critical signaling hub for coordinating nutrient uptake, fuel utilization, and thermogenic gene expression. These data provide a foundation for future studies into the mTORC2-FoxO1 signaling axis in different metabolic tissues and physiological conditions.
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Hung, Chien-Min. "mTORC2 Promotes Lipid Storage and Suppresses Thermogenesis in Brown Adipose Tissue in Part Through AKT-Independent Regulation of FoxO1: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/845.
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Recent studies suggest adipose tissue plays a critical role in regulating whole body energy homeostasis in both animals and humans. In particular, activating brown adipose tissue (BAT) activity is now appreciated as a potential therapeutic strategy against obesity and metabolic disease. However, the signaling circuits that coordinate nutrient uptake and BAT function are poorly understood. Here, I investigated the role of the nutrient-sensing mTOR signaling pathway in BAT by conditionally deleting Rictor, which encodes an essential component of mTOR Complex 2 (mTORC2) either in brown adipocyte precursors or mature brown adipocytes. In general, inhibiting BAT mTORC2 reduces glucose uptake and de novo lipogenesis pathways while increases lipid uptake and oxidation pathways indicating a switch in fuel utilization. Moreover, several key thermogenic factors (Ucp1, Pgc1α, and Irf4) are elevated in Rictor-deficient BAT, resulting in enhanced thermogenesis. Accordingly, mice with mTORC2 loss in BAT are protected from HFD-induced obesity and metabolic disease at thermoneutrality. In vitro culture experiments further suggest that mTORC2 cell-autonomously regulates the BAT thermogenic program, especially Ucp1 expression, which depends on FoxO1 activity. Mechanistically, mTORC2 appears to inhibit FoxO1 by facilitating its lysine-acetylation but not through the canonical AKT-mediated phosphorylation pathway. Finally, I also provide evidence that β-adrenergic signaling which normally triggers thermogenesis also induces FoxO1 deacetylation in BAT. Based on these data, I propose a model in which mTORC2 functions in BAT as a critical signaling hub for coordinating nutrient uptake, fuel utilization, and thermogenic gene expression. These data provide a foundation for future studies into the mTORC2-FoxO1 signaling axis in different metabolic tissues and physiological conditions.
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Centurión, Patricio, Ronald Gamarra, Gonzalo Caballero, Paul Kaufmann, and Pia Delgado. "Optimizing harvesting for facial lipografting with a new photochemical stimulation concept: One STEP technique™." Springer Science and Business Media Deutschland GmbH, 2020. http://hdl.handle.net/10757/655506.
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Background: Facial fat grafting for rejuvenation is one of the most popular facial aesthetic procedures in plastic surgery. It is always challenging and since there are a lot of techniques for adipose tissue (AT) harvesting, there are no standard procedures that guarantee natural and long-lasting results. We developed the selective tissue engineering photo stimulation technique (One STEP™) in which we used a novel infrared 1210-nm wavelength laser diode for fat preserved harvesting and direct fat injection that we named PicoGraft™, with no fat manipulation. Methods: This is a retrospective descriptive study in which we included all senior author’s patients that got facial fat grafting using the One STEP™ technique. We compared the AT aspirated, after laser emission (STEP-PicoGraft) and the standard assisted liposuction samples (SAL) in cultures. We study the mitochondrial activity of the ASC between STEP and SAL in fresh samples and after 24 h. The evaluation of the results included subjective changes regarding wrinkles, grooves, palpebral bags, hyperchromic spots, and fat hypotrophy of our patients. Results: Between July 2013 and May 2018, a total of 245 patients underwent facial fat grafting using this novel technique. We observed adipocytes preserved after STEP harvesting comparing morphologic changes in SAL samples with a high concentration of inflammatory particles in cultures. ASC mitochondrial activity shows an important difference of more than 7 times in STEP samples in fresh analysis that increase 12 times in 24 h. The subjective results show a good improvement in the periorbital area. The changes on the skin and subcutaneous tissue are seen from the second month and continue to improve up to 12 months. Conclusions: Facial fat grafting using the PicoGraft™ obtained by One STEP™ technique gives excellent volumetric and regenerative results in a single treatment without volumetric hypercorrection, and it is a good alternative for facial rejuvenation. The fat graft obtained with this novel technique is homogenous, without lumps, and has high concentration of viable stimulated ADSC and a high number of viable adipocytes. Level of evidence: Level III, therapeutic study.Revisión por pares
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Hsiao, Wen-Yu. "The Lipid Handling Capacity of Subcutaneous Fat Requires mTORC2 during Development." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1087.
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Overweight and obesity are associated with Type 2 Diabetes, non-alcoholic fatty liver disease, cardiovascular disease and cancer, but all fat is not equal as storing excess lipid in subcutaneous white adipose tissue (SWAT) is more metabolically favorable than in visceral fat. Here, we uncover a critical role for mTORC2 in setting SWAT lipid handling capacity. We find that subcutaneous white preadipocytes differentiating without the essential mTORC2 subunit Rictorexpress mature adipocyte markers but develop a striking lipid storage defect. In vivo,this results in smaller adipocytes, reduced tissue size, lipid re-distribution to visceral and brown fat, and sex-distinct effects on systemic metabolic fitness. Mechanistically, mTORC2 promotes transcriptional upregulation of select lipid metabolism genes controlled by PPARgand ChREBP. These include genes that control lipid uptake, synthesis, and degradation pathways as well as Akt2, the gene encoding its substrate and insulin effector. Finally, we reveal a potential novel mTORC2 target, ACSS2, which might control intracellular acetyl-CoA availability and regulate metabolic gene expression by altering histone modification in white adipocytes. Exploring this pathway may uncover strategies to promote safe lipid storage and improve insulin sensitivity.
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Silvério, Renata. "A modulação da lipase de triacilglicerol do adipócito (ATGL) e da perilipina 1 contribui para o aumento da lipólise em pacientes caquéticos." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-24052012-084649/.
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A depleção de tecido adiposo é um marcador da caquexia. Neste contexto, o aumento na lipólise decorrente do aumento na expressão da lipase hormônio-sensível (LHS) parece ser o fator-chave. Entretanto, a contribuição das novas proteínas relacionadas à lipólise [adipose triglyceride lipase (ATGL), comparative gene identification 58 (CGI-58) e perilipina] ainda é controversa. Caracterizamos a expressão destas proteínas e de adipocinas na caquexia. Pacientes com câncer caquéticos foram investigados. Um modelo experimental foi também estudado utilizando animais portadores de tumor sacrificados no 7º (TB7) e no 14º dia (TB14) após a inoculação tumoral e controles. Foram analisados no tecido adiposo os aspectos morfológicos, morfométricos e moleculares. Verificamos nos pacientes um aumento na expressão de LHS e ATGL, concomitantemente à redução da perilipina. Nos animais TB7 verificou-se um desequilíbrio na secreção de fatores anti e pró-inflamatórios e no grupo TB14 houve redução na expressão das proteínas analisadas sugerindo comprometimento da função celular.Loss of fat mass is a hallmark of cachexia. It seems that an increase in lipolysis due to increased expression of hormone-sensitive lipase (HSL) is the key factor behind this effect. However, the contribution of novel proteins related to lipolysis [adipose triglyceride lipase (ATGL), comparative gene identification - 58 (CGI-58) and perilipin 1] is still controversial. We characterized the expression of those proteins and adipokines in cachexia. Subcutaneous adipose tissue from cachetic cancer patients and epidydimal pad from tumour-bearing rats was analysed. Morphological, morphometric and molecular aspects were examined. We found an increased HSL and ATGL expression and reduction in perilipin 1 content in cachectic patients. In rats, at the intermediate stage of the syndrome, there was an imbalance in the secretion of pro and anti-inflammatory factors. In terminal cachexia the expression of almost all proteins analysed was reduced in the animals, suggesting impairment of cellular function.
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Murrieta, Charles M. "Lipogenic enzyme mRNA of milk and adipose tissue of lactating beef cows and their calves influence of day of lactation, maternal dietary fat supplementation, and body condition score /." Laramie, Wyo. : University of Wyoming, 2007. http://proquest.umi.com/pqdweb?did=1338900371&sid=1&Fmt=2&clientId=18949&RQT=309&VName=PQD.
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Foster, Michelle Tranace. "Central Nervous System Regulation of Fat Cell Lipid Mobilization: The Role of the Sympathetic Nervous System." Digital Archive @ GSU, 2006. http://digitalarchive.gsu.edu/biology_diss/2.
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Obesity is a growing disorder in the United States, affecting over 60% of the population. We previously defined sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT) using a viral transneuronal tract tracer. SNS innervation of WAT is the principle initiator of lipolysis, whereas decreases in sympathetic drive promote lipid accumulation. Which of the many origins of SNS outflow from brain to WAT results in SNS-mediated changes in lipid mobilization (increases in drive) or accumulation (decrease in drive) is unknown. Previous research indicates that sympathetic denervation blocks lipid mobilization; thus, rostral sites in the neuroaxis connected to WAT via the SNS may promote WAT lipid mobilization. The hypothalamic paraventricular nucleus (PVN) may play a role via its descending projections to the intermediolateral horn of the spinal cord. Therefore, the consequences of PVN lesions (PVNx) on WAT mobilization or accumulation were tested. PVNx resulted in increased lipid accumulation, indicated by increases in retroperitoneal (RWAT) , epididymal (EWAT) , and inguinal WAT (IWAT) pad masses, in fed hamsters, but PVNx did not block fasting (56 h)-induced lipid mobilization. Because adrenal medullary catecholamines, especially epinephrine, also play a minor role in lipid mobilization, we tested the contribution of catecholamine release on lipid mobilization through adrenal demedullation (ADMEDx), with and without PVNx, and found fastinginduced lipid mobilization was not blocked. There was, however, a suggestion that distal denervation of IWAT, with and without ADMEDx, partially blocked lipid mobilization. In addition, evidence suggests SNS also may be an important controller of fat cell proliferation. Surgical denervation of WAT triggers increases in fat cell number (FCN), but have not determined if this FCN increase is due to preadipocyte proliferation or differentiation of preadipocytes into mature fat cells. We also have not demonstrated what role sensory innervation may have in regulating white adipocyte proliferation. Therefore, the role of WAT sympathetic or sensory innervation on adipocyte proliferation was tested. The SNS but not sensory denervation triggered bona fide proliferation as indicated by bromodeoxyuridine plus AD3, a specific adipocyte membrane protein, colabeling. These and previous data suggest that the SNS plays a role in regulating adiposity.
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May, Stéphanie [Verfasser], Thomas [Akademischer Betreuer] Skurk, and Dirk [Akademischer Betreuer] Haller. "Influence of adipogenesis and high fat diet on the development of cell stress markers in adipose tissue / Stephanie May. Gutachter: Dirk Haller ; Thomas Skurk. Betreuer: Thomas Skurk." München : Universitätsbibliothek der TU München, 2013. http://d-nb.info/104744092X/34.
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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.
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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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Yamada, Mônica. "Efeito da ingestão do extrato aquoso de erva-mate (Ilex paraguariensis) sobre a resposta inflamatória do tecido adiposo branco de ratos alimentados com ração hiperlípidica." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-23052013-105359/.
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Introdução - A dieta hiperlipídica é uma das principais causas da obesidade, provocando importantes alterações metabólicas, como aumento de gordura corporal, dislipidemia e resistência à ação da insulina. Além disso, a obesidade gera um quadro inflamatório crônico e de baixa intensidade no tecido adiposo branco, que é caracterizado pela ativação de vias inflamatórias, como a via do fator de transcrição nuclear kappa B (NF-kB), que é responsável pela transcrição de genes com ação pró-inflamatória, como o fator de necrose tumoral (TNF)-alfa e a proteína quimiotática para monócitos (MCP)-1. A erva-mate (Ilex paraguariensis) contém compostos bioativos, como o ácido clorogênico, a quercetina e o kaempferol, os quais apresentam a capacidade de modular a expressão de genes envolvidos na resposta inflamatória. Objetivo - Investigar o efeito da ingestão do extrato aquoso de erva-mate sobre os parâmetros metabólicos e sobre a resposta inflamatória no tecido adiposo branco de ratos alimentados com ração hiperlipídica. Material e métodos - Ratos machos Wistar foram submetidos à ração controle ou hiperlipídica por 12 semanas. Após esse período, 12 animais de cada grupo foram eutanasiados, constituindo os grupos baseline. O restante dos animais foi distribuído em quatro grupos que receberam, por gavagem, o extrato aquoso de erva-mate (1 g/kg massa corporal/dia) ou água, durante quatro semanas. Após esse período, todos os animais foram eutanasiados. Durante a 12a e a 16a semana do protocolo experimental, os animais foram submetidos ao teste oral de tolerância à glicose e ao teste intraperitoneal de tolerância à insulina. A partir do sangue, foram determinadas as concentrações de glicose, de insulina e de biomarcadores inflamatórios, bem como o perfil lipídico. A composição corporal foi determinada por meio da análise química da carcaça. A partir do tecido adiposo periepididimal, foi avaliada a expressão das proteínas chaves envolvidas na inflamação crônica e na resistência à ação da insulina, por Western blot, bem como a expressão gênica de adipocinas por PCR em tempo real. Resultados - A ração hiperlipídica provocou aumento da adiposidade, alteração do perfil lipídico, intolerância à glicose e inflamação sistêmica. No tecido adiposo periepididimal, a ração hiperlipídica provocou redução da fosforilação da AKT nos animais estimulados agudamente com insulina. A ingestão do extrato aquoso de erva-mate, por quatro semanas, reduziu o ganho de peso corporal e melhorou o perfil lipídico nos animais alimentados com a ração hiperlipídica em relação ao correspondente grupo tratado com água. Contudo, o extrato aquoso de erva-mate não foi capaz de reverter as demais alterações metabólicas provocadas pela ingestão da ração hiperlipídica. Conclusão - A ingestão da ração hiperlipídica promoveu alterações metabólicas, todavia, não induziu inflamação crônica no tecido adiposo periepididimal. Por outro lado, a ingestão do extrato aquoso de ervamate foi capaz de reduzir o ganho de peso corporal e melhorar o perfil lipídico dos animais que consumiram a ração hiperlipídicaIntroduction - High-fat diet is one of the main causes of obesity, inducing significant metabolic changes, such as increased fat mass, dyslipidemia and insulin resistance. Furthermore, obesity is associated with a chronic state of low-grade inflammation in white adipose tissue, which is characterized by activation of inflammatory pathways, like nuclear factor kappa B (NF-kB) pathway, implicated in the transcription of many genes with pro-inflammatory action, such as tumor necrosis factor (TNF)-alpha and monocyte chemotatic protein (MCP)-1. Yerba mate (Ilex paraguariensis) contains bioactive compounds, such as chlorogenic acid, quercetin and kaempferol that have the ability to modulate genes envolved in inflammatory response. Objective - To investigate the effect of yerba mate aqueous extract consumption on metabolic parameters and on inflammatory response in white adipose tissue of high-fat diet-fed rats. Material and methods - Male Wistar rats were submitted a control or a high-fat diet for 12 weeks. After this period, 12 rats of each group were euthanized, constituting the baseline groups. The remainder animals were distributed into four groups, which received by intragastric gavage the yerba mate aqueous extract or vehicle (1 g/kg body weight/day) for four weeks and then, all animals were euthanized. Oral glucose and intraperitoneal insulin tolerance tests were performed at 12 and 16 weeks of experimental protocol. Blood glucose, insulin, lipid profile and inflammatory markers were measured. Water, lipid, protein and ash content were analyzed by carcass chemical composition. Periepididymal adipose tissue were employed to evaluate key proteins involved in inflammatory and insulin signaling pathway by Western blot, and adipokines gene expression by real time PCR. Results - High-fat diet induced body adiposity, dyslipidemia, glucose intolerance and systemic inflammation. In periepididymal fat, high-fat diet decreased AKT phosphorylation in rats acutelly stimulated with insulin. The consumption of yerba mate aqueous extract for four weeks reduced body weight gain and improved lipid profile in high-fat diet group compared to non-treated group. However, yerba mate did not repair others dysfunctions induced by high-fat feeding. Conclusion - High-fat feeding produced some metabolic dysfunctions, but did not induce chronic inflammation in periepididymal adipose tissue. On the other hand, the yerba mate aqueous extract consumption reduced body weight gain and improved lipid profile of rats fed a high-fat diet