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Bickerton, Alex Sam Thomas. "Fat metabolism and the metabolic syndrome". Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:9108a8ca-8b3e-4e45-98e2-4765c009774f.
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Background: The metabolic syndrome is associated with an increased risk of diabetes and vascular disease. In order to understand the pathophysiological processes underlying such risk, it is necessary to develop a better understanding of normal fat metabolism and abnormalities associated with the syndrome. The hypothesis tested in this thesis is that specific abnormalities in adipose tissue and muscle fat metabolism characterise the metabolic syndrome. Methods: Fasting biochemical parameters were measured in a cohort of overweight men with and without the metabolic syndrome. Stable-isotope labeling and arterio-venous difference measurements were conducted in 18 men to elucidate pathways of exogenous and endogenous fat metabolism under fasting and postprandial conditions in adipose tissue and skeletal muscle. In addition, a pilot study of the effects of heat and electrical stimulation on adipose tissue metabolism was undertaken. Results: Cohort study - The prevalence of the metabolic syndrome depended on the definition used. Total cholesterol and apoB were greater in those with the metabolic syndrome than in those without. There was no difference in fasting NEFAs. Metabolic investigation - There was significant postprandial uptake of NEFA from the circulating NEFA pool by adipose tissue. Chylomicrons were confirmed as the preferred substrate of LPL. There was preferential uptake of FAs derived from chylomicron hydrolysis. There was release of NEFA across muscle. In the metabolic syndrome, adipose tissue NEFA output is lower during fasting and falls less following a meal than in the healthy obese. Clearance of dietary-derived TG is lower across both adipose tissue and muscle in the metabolic syndrome. Pilot study – Heat increased measures of lipolysis whereas electrical stimulation had no effect. Conclusions: Fat metabolism in individuals with the metabolic syndrome is characterised by metabolic inflexibility but not insulin resistance.
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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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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.
4
Orme, Elizabeth Catherine. "Fat metabolism in the exercising thoroughbred horse". Thesis, Open University, 1995. http://oro.open.ac.uk/57558/.
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The thoroughbred horse has been selectively bred for speed and has a high capacity for carbohydrate metabolism. The following series of studies investigated the relative contribution of fat and carbohydrate to energy production during exercise of varying intensity. Furthermore the work assessed the capacity of the horse to increase the contribution of fat to energy production as the result of either an acute increase in the availability of plasma free fatty acids (FFA) or as the result of chronic fat supplementation. Finally an adaptational response to feeding a fat supplemented diet was described. The variation in plasma long chain FFA over a 24 hour period was described. The early hours of the morning represented the period of greatest variability in plasma FFA concentration. This period was characterised by a significant increase in total and individual FFA concentration, which was unrelated to feed intake. As a result of the reported circadian rhythm in plasma FFA all subsequent exercise studies were performed during the period of least variability in plasma FFA concentration. A model for the pre-exercise elevation of plasma FFA, using a combination of a triglyceride emulsion and the heparinoid type substance pentosan polysulphate, was used to investigate the effect of increased FFA availability on fat utilisation during prolonged low intensity exercise. Pentosan polysulphate was used in preference to heparin following an investigation of their relative lipolytic and anticoagulative properties. Pentosan polysulphate when administered at 3 times the dose of heparin resulted in a comparable increase in plasma total lipase activity. When co-administered with a triglyceride emulsion, pentosan polysulphate resulted in a similar increase in plasma FFA concentration relative to that produced with the same triglyceride emulsion and heparin. The anticoagulative effect of pentosan polysulphate, however, was approximately 9 times less than that of heparin, as measured by activated partial thromboplastin time. The contribution of fat and carbohydrate to energy production during exercise was influenced by both the intensity and duration of exercise, as indicated by measurements of respiratory exchange ratio (RER). The inter-horse variability in RER was greatest during low intensity exercise. An increase in the contribution of carbohydrate to energy production occurred at the onset and during the early stages of prolonged exercise and as the result of an increase in exercise intensity. A proportion of horses exhibited an increase in the utilisation of fat during low intensity prolonged exercise as a result of a pre-exercise elevation in plasma FFA concentration. RER was consistently lower during exercise in 5 out of the 7 horses studied following a pre-exercise elevation of plasma FFA. Furthermore, plasma glucose concentration was elevated above that observed during the control session in 4 of these 5 horses for at least the first 15 minutes of exercise. A prolonged period of fat supplementation resulted in an improved management of the fat load. Following 10 weeks of dietary treatment a significant increase in plasma cholesterol concentration and a significant decrease in plasma triglyceride concentration was reported. The decrease in plasma triglyceride concentration was associated with a mean 50% increase in post pentosan polysulphate plasma total lipase activity. It is suggested that the increase in the post pentosan polysulphate plasma total lipase activity may have reflected an increase in muscle lipoprotein lipase activity. A significant increase in the activity of muscle citrate synthase was observed during the period of fat supplementation. No significant change occurred in muscle ß-hydroxyacyl CoA dehydrogenase activity or in the concentration of resting muscle glycogen and triglyceride as a result of fat supplementation. RER was significantly lower in the latter stages of prolonged low intensity exercise, during the period of fat supplementation, relative to the same exercise performed before the introduction and following 5 weeks of withdrawal of the fat supplemented diet. The reduction in RER during the period of fat supplementation was associated with a greater exercise induced increase in plasma FFA concentration. The above differences were also apparent during moderate intensity exercise, although, examination of the individual horse data revealed that the effect was not as clear as that observed during low intensity exercise. No significant differences were reported in either RER or plasma FFA concentration in response to moderate/high intensity exercise during the period of fat supplementation. Neither were any significant differences observed in either RER or plasma FFA concentration in the control group at any exercise intensity. An increased availability of plasma FFA and an increase in the oxidative capacity of muscle, as well as an enhanced ability to utilise plasma triglycerides may have contributed to the increase in fat utilisation, observed during low and moderate intensity exercise, in response to fat supplementation. The effect of differences in the hormonal response to a fat supplemented diet as a precipitant of the observed adaptational responses in these studies requires further investigation.
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Osei, Michael. "A study of dietary fat metabolism in healthy and insulin resistant subjects". Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708531.
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Olenick, Alyssa. "Metabolic Flexibility Among Women after a Single High Fat Meal". TopSCHOLAR®, 2017. http://digitalcommons.wku.edu/theses/1970.
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PURPOSE: Obese women have increased rates of metabolic diseases compared to those of healthy weight status. Additionally, African-American (AA) women have higher rates of metabolic disease compared to Caucasian (CA) women. Metabolic inflexibility is the inability to adjust substrate oxidation in response to dietary intake; potentially leading to weight gain and the development of metabolic disease. Few studies have investigated the impact of weight status and/or ethnicity on the metabolic response of women to a single high fat meal. An acute unfavorable metabolic response may contribute to the higher incidence of metabolic disease among not only obese, but also AA women. Therefore, the purpose of this study was to determine the impact that weight status (lean vs. overweight/obese) and/or ethnicity (CA vs. AA) has on metabolic health in women in response to a single high fat meal. METHODS: CA (n= 15; age=26.27±5.65 yrs; BMI=30.72±11.92kg/m2) and AA (n= 12; age=26.75±6.65yrs; BMI=28.32±6.91kg/m2) women consumed a high fat shake (1062 calories, 56% fat). Blood was drawn and resting energy expenditure (REE) and substrate oxidation (estimated using indirect calorimetry) were assessed at baseline/fasted (T1), 120 minutes post-shake, (T2) 240 minutes post-shake (T3). RESULTS: Lipid and carbohydrate oxidation significantly increased among all women in response to the high fat meal (p<0.01). Significant increases in fat oxidation were seen from T1-T2 for all women (CA lean: +57.9±24.5%; CA overweight/obese: +30.2±11.8%; AA lean: +10.2±18.1%; AA overweight/obese: +40.6±52.6%; p<0.01). Among the CA women only, CA lean women displayed a significantly higher increase in fat oxidation in response to the meal compared to CA overweight/obese women, but there were no differences among lean and overweight/obese AA women. Similarly, weight status influenced changes in apolipoproteins after consuming the high fat meal among CA women, but not AA women. CONCLUSIONS: CA lean women displayed the most metabolic flexibility in response to the high fat meal. A metabolic system that is less able to respond to metabolic stimuli such as a high fat diet (as noted in all groups compared to lean CA women) may play a role in the increased metabolic disease prevalence among obese and AA women.
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Jeukendrup, Asker Erik. "Aspects of carbohydrate and fat metabolism during exercise". Haarlem : Maastricht : De Vrieseborch ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=6815.
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Brandt, Karsten. "Fat metabolism and the control of food intake". Hamburg Kovač, 2006. http://www.verlagdrkovac.de/3-8300-2648-X.htm.
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Grohmann, Malcolm James. "Regulation of children's fat and skeletal muscle metabolism". Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422554.
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Gill, Jason Martin Regnald. "Postprandial studies of moderate exercise and triacylglycerol metabolism". Thesis, Loughborough University, 1999. https://dspace.lboro.ac.uk/2134/11106.
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Exaggerated postprandial lipaemia has been implicated in the development of atherosclerosis. Thus, by reducing postprandial TAG concentrations, exercise may play a role in delaying atherogenic progression. This thesis sought to explore the qualitative nature of, and the mechanisms behind, the moderate exercise-induced attenuation to postprandial lipaemia. Before the experimental studies commenced, a reproducibility study was undertaken. This showed that in a group of eight middle-aged men, the postprandial plasma TAG response differed by only 1.9 ± 5.1 % (mean ± standard error) on a testretest basis, indicating that the oral fat tolerance test had enough precision to detect the effect of exercise on TAG metabolism. Previous work suggested that the exercise-induced reduction to lipaemia was linked to the energy expended by exercise. As the attenuation may have been mediated by energy deficit, rather than exercise per se, a study comparing the effect of a 90-minute moderate exercise session with an equivalent dietary-induced energy deficit on postprandial lipid metabolism was undertaken, in a group of eleven postmenopausal women. This showed that the reduction in postprandial lipaemia elicited by exercise was far greater than that elicited by intake-restriction (20 % vs. 7 %). The second experimental study aimed to establish the effect of a 90-minute moderate exercise session on postprandial chylomicron- and very-Iow-density lipoprotein (VLDL)-TAG concentrations, and its effect on exogenous (through use of a l3e-Iabelled lipid) and endogenous fat oxidation, in a group oftwelve middle-aged men. Exercise reduced postprandial lipaemia by 23 %, and over three-quarters of this reduction was due to lower VLDL-TAG concentrations. Increases in endogenous fat oxidation accounted for over half of the increase in postprandial fat oxidation. In the third experimental study, the effect of a 90-minutes moderate exercise session on Intralipid clearance, and postprandial lipaemia, was determined in a group of eight middle-aged men. Exercise attenuated postprandial lipaemia by 18 %, but did not increase Intralipid clearance. Taken together, these data imply that moderate exercise predominantly reduced postprandial TAG concentrations by reducing hepatic VLDL secretion, rather than increasing TAG clearance, and this effect is not mediated by whole-body energy deficit. In addition, this work has shown that moderate exercise is effective at attenuating postprandial lipaemia in middle-aged men and postmenopausal women.
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Roper, J. F. D. "The effect of fat encapsulation on the fate of labile nutrients in the ruminant gut". Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378358.
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Lewandowski, Paul, i 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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Faraj, May. "Postprandial plasma acylation stimulating protein response and fat metabolism in post-obese women". Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=29889.
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Acylation stimulating protein (ASP) is a plasma protein that significantly increases adipose tissue fat storage. In vivo and in vitro studies have suggested a role for plasma ASP in enhancing postprandial plasma triglyceride (TG) clearance. The primary objective of this study was to examine, for the first time, the postprandial response of plasma ASP and the fate of an exogenous fat source in 8 post-obese and 8 matched control women. This was done through following 13C-labeled high fat breakfast meal (1062 Cal, 67% fat) every 2 hours for 8 hours in 3 plasma pools and in expired breath CO2. The 3 plasma pools were: TG fraction in triglyceride rich lipoproteins (TRL) with sedimentation factor Sf > 400 (referred to as chylomicron-TG), TG fraction in TRL with Sf = 20--400 (referred to as VLDL-TG), and plasma free fatty acid (FFA). The secondary objective was to examine fasting and postprandial resting energy expenditure (REE), thermic effect of food (TEF), carbohydrate to fat oxidation rate and insulin sensitivity, which are factors that have been implicated in the tendency of post-obese women to regain weight. (Abstract shortened by UMI.)
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Asante, Emmanuel A. "Biochemical genetics of lipid metabolism in chickens and mice". Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/11520.
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Kimber, Nicholas E., i mikewood@deakin edu au. "Skeletal muscle fat metabolism during post-exercise recovery in humans". Deakin University. School of Exercise and Nutrition Sciences, 2004. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050826.115311.
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Recovery after prolonged or high-intensity exercise is characterised by a substantial increase in adipose tissue lipolysis, resulting in elevated rates of plasma-derived fat oxidation. Despite the large increase in circulating fatty acids (FAs) after exercise, only a small fraction of this is taken up by exercised muscle in the lower extremities. Indeed, the predominant fate of non-oxidised FAs derived from post-exercise lipolysis is reesteriflcation hi the liver. During recovery from endurance exercise, a number of changes also occur hi skeletal muscle that allow for a high metabolic priority towards glycogen resynthesis. Reducing muscle glycogen during exercise potentiates these effects, however the cellular and molecular mechanisms regulating substrate oxidation following exercise remain poorly defined. The broad arm of this thesis was to examine the regulation of fat metabolism during recovery from glycogen-lowering exercise hi the presence of altered fat and glucose availability. In study I, eight endurance-trained males completed a bout of exhaustive exercise followed by ingestion of carbohydrate (CHO)-rich meals (64-70% of energy from CHO) at 1, 4, and 7 h of recovery. Duplicate muscle biopsies were obtained at exhaustion and 3, 6 and 18 h of recovery. Despite the large intake of CHO during recovery (491 ± 28 g or 6.8 + 0.3 g kg-1), respiratory exchange ratio values of 0.77 to 0.84 indicated a greater reliance on fat as an oxidative fuel. Intramuscular triacylglycerol (IMTG) content remained unchanged in the presence of elevated glucose and insulin levels during recovery , suggesting IMTG has a negligible role in contributing to the enhanced fat oxidation after exhaustive exercise. It appears that the partitioning of exogenous glucose towards glycogen resynthesis is of high metabolic priority during immediate post-exercise recovery, supported by the trend towards reduced pyruvate dehydrogenase (PDH) activity and increased fat oxidation. The effect of altering plasma FA availability during post-exercise recovery was examined in study II. Eight endurance-trained males performed three trials consisting of glycogen-lowering exercise, followed by infusion of either saline (CON), saline + nicotinic acid (NA) (LFA) or Intralipid and heparin (HFA). Muscle biopsies were obtained at the end of exercise (0 h) and at 3 and 6 h in recovery. Altering the availability of plasma FAs during recovery induced changes in whole-body fat oxidation that were unrelated to differences in skeletal muscle malonyl-CoA. Furthermore, fat oxidation and acetyl-CoA carboxylase (ACC) phosphorylation appear to be dissociated after exercise, suggesting mechanisms other than phosphorylation-mediated changes in ACC activity have an important role in regulating malonyl-CoA and fat metabolism in human skeletal muscle after exercise. Alternative mechanisms include citrate and long-chain fatty acyl-CoA mediated changes in ACC activity, or differences in malonyl-CoA decarboxylase (MCD) activity. Reducing plasma FA concentrations with NA attenuated the post-exercise increase in MCD and pyruvate dehydrogenase kinase 4 (PDK4) gene expression, suggesting that FAs and/or other factors induced by NA are involved hi the regulation of these genes. Despite marked changes hi plasma FA availability, no significant changes in IMTG concentration were detected, providing further evidence that plasma-derived FAs are the preferential fuel source contributing to the enhanced fat oxidation post-exercise during recovery. To further examine the effect of substrate availability after exercise, Study III investigated the regulation of fat metabolism during a 6 h recovery period with or without glucose infusion. Enhanced glucose availability significantly increased CHO oxidation compared with the fasted state, although no differences in whole-body fat oxidation were apparent. Consistent with the similar rates of fat metabolism, no difference hi AMPK or ACCβ phosphorylation were observed between trials. In addition, no significant treatment or time effects for IMTG concentration were detected during recovery. The large exercise-induced PDK4 gene expression was attenuated when plasma FAs were reduced during glucose infusion, supporting the hypothesis that PDK4 is responsive to sustained changes in lipid availability and/or changes in plasma insulin. Furthermore, the possibility exists that the suppression of PDK4 mRNA also reduced PDK activity and thus maintained PDH activity to account for the higher rates of CHO oxidation observed during glucose infusion compared with the control trial.
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Sonko, Bakary Jallow. "Studies of carbohydrate and fat oxidation in human energy metabolism". Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240088.
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Greathead, Henry M. R. "Fat and protein metabolism in cattle fed on grass silage". Thesis, University of Nottingham, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339657.
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Thapa, Gita. "Developmental Changes in Fat Metabolism of Tobacco Hornworm, Manduca Sexta". Thesis, North Dakota State University, 2012. https://hdl.handle.net/10365/26632.
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Insects fed high carbohydrate diets have increased fat storage, and excess fat storage in insects may have fitness costs. M. sexta larvae reared on 5.6% fat diet had lower body mass and growth rate compared to those on 3.4% fat or 0.4% fat diets. Fifth instar caterpillars fed high-fat diet ate less food but had higher approximate digestibility than the low-fat diet fed caterpillars. Analysis of fat body and fecal pellet lipid content showed high-fat diet fed caterpillars stored and excreted more lipids than low-fat diet fed caterpillars. To test the hypothesis that increased dietary fat alters lipid transport, we measured mRNA expression of apolipoproteins I and II, proteins for transporting lipids. Expression of apolipoproteins I and II did not differ with dietary fat. Negative feedback from fat intake could inhibit feeding via endocrine pathways. This research will increase our understanding of the regulation of feeding in caterpillars.
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Yang, Yan. "CEACAM1: A Molecular Link Between Fat Metabolism and Insulin Clearance". University of Toledo Health Science Campus / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=mco1115060085.
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Fujitani, Mina. "Studies on the regulation of fat metabolism during endurance exercise". Kyoto University, 2015. http://hdl.handle.net/2433/199366.
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Kyoto University (京都大学)0048
新制・課程博士
博士(農学)
甲第19042号
農博第2120号
新制||農||1032(附属図書館)
学位論文||H27||N4924(農学部図書室)
31993
京都大学大学院農学研究科食品生物科学専攻
(主査)教授 伏木 亨, 教授 保川 清, 教授 金本 龍平
学位規則第4条第1項該当
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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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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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Bennoson, Janet. "The effect of manipulating the macronutrient composition of meals postprandial lipid metabolism". Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310698.
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Baugh, Mary Elizabeth. "Skeletal Muscle Substrate Metabolism following a High Fat Diet in Sedentary and Endurance Trained Males". Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/85417.
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Insulin resistance (IR), T2DM, and obesity together form a cluster of interrelated metabolic challenges that may be linked by metabolic inflexibility. Metabolic inflexibility is characterized by the resistance to switching substrate oxidation preference based on substrate availability and can be measured in either fasted or insulin-stimulated conditions. As the largest site for glucose disposal and a primary tissue influencing regulation of blood glucose concentrations, skeletal muscle likely plays a central role in regulating substrate oxidation preference based on substrate availability. Skeletal muscle lipotoxicity caused by an impaired regulation of fat uptake and oxidation is postulated to disrupt insulin signaling and lead to skeletal muscle IR. High dietary saturated fat intake results in reduced basal fat oxidation and a resistance to switching to carbohydrate oxidation during insulin-stimulated conditions in susceptible individuals. This metabolic inflexibility may lead to an accumulation of intramyocellular species that impair insulin signaling. Endurance exercise training improves the capacity for fat oxidation in metabolically inflexible individuals. However, relatively little is known about how endurance exercise training influences substrate oxidation preference when paired with a high fat diet (HFD). Therefore, the purpose of this study was to determine the effects of a HFD on substrate metabolism in skeletal muscle of sedentary and endurance trained (ET) males. Healthy, sedentary (n=17) and ET (n=7) males first consumed a 10-day moderate carbohydrate diet (55% carbohydrate, 30% total fat, <10% saturated fat) isocaloric to their individual energy requirements and then underwent a 4- hour high fat challenge testing session. During the session, they consumed a high fat meal (820 kcals; 25% carbohydrate, 63% total fat [26% saturated fat]), and skeletal muscle biopsies were taken in the fasted and 4-hour postprandial conditions. Participants then consumed a 5-day HFD (30% carbohydrate, 55% total fat, 25% saturated fat) and repeated the high fat challenge testing session. Substrate oxidation measures were performed on the collected skeletal muscle tissue, and the meal effect, defined as the percent change from the fasting to 4- hour postprandial condition, for each measure was calculated. There was a HFD by physical activity group interaction on meal effect for metabolic flexibility (P<0.05) and a HFD effect on meal effect for glucose oxidation (P<0.05). Meal effects for metabolic flexibility and glucose oxidation were maintained in the ET (20 ± 4% to 41 ± 21% and 128 ± 92% and 41 ± 15%, respectively; both P>0.05) but decreased in the sedentary (34 ± 7% to 4 ± 5% and 78 ± 26% to -21 ± 6%, respectively; both P<0.01) group. There were trends toward HFD effects on reductions in meal effects for total (P=0.062) and incomplete (P=0.075) fat oxidation, which were driven primarily by an increase in fasting total (12.1 ± 2.6 nmol/mg protein/h to 18.5 ± 2.3 nmol/mg protein/h; P<0.01) and incomplete (11.5 ± 2.5 nmol/mg protein/h to 17.6 ± 2.3 nmol/mg protein/h; P<0.01) fat oxidation in the ET group as a result of the HFD. Fasting total and incomplete fat oxidation did not change in the sedentary group (7.3 ± 0.8 nmol/mg protein/h to 7.8 ± 0.8 nmol/mg protein/h and 6.8 ± 0.7 nmol/mg protein/h to 7.2 ± 0.8 nmol/mg protein/h, respectively; both P>0.05). Overall, these findings suggest the ET state attenuates deleterious effects of a short-term HFD on reduced metabolic flexibility and insulin-stimulated glucose oxidation. In addition, a HFD-induced reduction in fat oxidation during the fasted-to-fed transition may be caused by differing mechanisms in sedentary and ET individuals. These findings provide a basis for future work targeting the elucidation of potential mechanistic differences in substrate oxidation preference between sedentary and ET individuals.Ph. D.
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Pufal, Deborah Ann. "The effects of two structural isomers of monopalmitoyl-dioleoylglycerol on lipoprotein metabolism". Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262108.
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Whitley, Helena Angela. "The interaction of dietary carbohydrate and fat at rest and during exercise". Thesis, Liverpool John Moores University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263546.
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Ip, P. M., i 葉沛汶. "Perinatal nutrition affects adiposity and skeletal muscle fat metabolism in rats". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30253111.
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Ka, Khady. "Fat and bone metabolism in relation to gingival inflammation in children". Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121433.
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Introduction: Epidemiological evidence suggests an association between diseases related to fat and bone metabolism and periodontal health. Despite the extensive evidence showing these associations in adults, only a few studies have been conducted in children. We address a gap in the pediatric literature by examining the extent to which markers of gingival inflammation are associated with i) metabolic syndrome (MetS) and: ii) plasma uncarboxylated osteocalcin (unOC). As a preliminary step, we first explore the extent to which whole-body bone measurements were associated with fat mass after taking into account the effect of lean mass. Methodology: The data used in this project derives from the QUALITY cohort, an ongoing longitudinal study investigating the natural history of obesity in children of Quebec, Canada. The QUALITY cohort includes 630 Caucasian children aged 8-10 years at cohort inception, with at least one obese biological parent. Participants were systematically recruited through schools located within 75 km of Montreal and Quebec City. In this thesis, we present cross-sectional analyses from the baseline visit using multiple linear regression analyses with adjustment for potential confounding variables. Whole-body bone mineral content (BMC, g), bone area (cm2), bone mineral density (BMD, g/cm2), lean mass (kg) and fat mass (kg) were measured by dual-energy X-ray absorptiometry (DXA). MetS was defined according to the International Diabetes Federation recommendations. Plasma unOC levels were determined by enzyme-linked immunosorbent assay. Gingival inflammation was defined by the level of gingival crevicular fluid (GCF) tumour necrosis factor alpha (TNF-α) and the extent of gingival bleeding. Results: Positive associations between fat mass and whole-body DXA bone measurements, including BMC, bone area and BMD, were observed after taking into account the effect of lean mass. Specifically, a 1-kg increase in fat was associated with 9.32 g (95% confidence interval [CI]: 7.26, 11.39), 8.02 cm2 (95%CI: 6.72, 9.32) and 0.002 g/cm2 (95%CI: 0.000, 0.002), increase in whole-body BMC, bone area and BMD respectively. Boys with MetS compared to those without, had a 49.5% (95%CI: 25.72, 73.22) higher GCF TNF-α level and 13.7% (95%CI: 1.1, 26.2) more sites with gingival bleeding. Moreover, for 3 of the 5 components of MetS – waist circumference, fasting plasma triglycerides and systolic blood pressure – an increase was associated with increased GCF TNF-α level in boys. No such findings were seen in girls. A 1-ng/ml increase in plasma unOC was associated with 0.96% decrease (95% CI: -1.69, -0.23) in GCF TNF-α level. Conclusion: Our results provide novel findings showing a clustering of metabolic abnormalities, low plasma unOC and high gingival inflammation among 8-10 Caucasian children. Moreover, they suggest that fat and bone metabolism may be associated with periodontal health as early as in childhood. Documenting the association of conditions related to fat and bone metabolism with periodontal health in children may have public health implications. This may allow identification of individuals at risk of developing several related conditions long before they develop clinically and implementation of early preventive measures.Introduction: Les données épidémiologiques suggèrent une association entre la santé parodontale et les maladies liées au métabolisme des graisses et des os. En dépit des nombreuses études montrant ces associations chez l'adulte, seules quelques études ont été menées chez l'enfant. Dans ce projet, nous avons tenté de combler une lacune dans la littérature pédiatrique en examinant dans quelle mesure des marqueurs de l'inflammation gingivale sont associées : 1) au syndrome métabolique (MetS) et 2) à la concentration plasmatique d'ostéocalcine non carboxylée (unOC). De plus, dans un premier temps, nous avons évalué la relation entre des mesures de santé osseuse et la masse grasse indépendamment de la masse maigre. Méthodologie: Dans ce projet, nous utilisons des données provenant de la cohorte QUALITY, une étude longitudinale portant sur l'histoire naturelle de l'obésité chez les enfants du Québec, au Canada. La cohorte QUALITY inclut 630 enfants de race blanche, âgés de 8-10 ans lors du recrutement, ayant au moins un parent biologique obèse. Les participants ont été recrutés dans les écoles situées à moins de 75 kilomètres de Montréal et de la ville de Québec. Dans cette thèse, nous présentons des analyses transversales de la visite initiale. Nous avons utilisé des régressions linéaires multiples avec ajustement pour les variables de confusion potentielles. La teneur minérale osseuse (BMC, g), la surface osseuse (cm2), la densité minérale osseuse (BMD, g/cm2), la masse maigre (kg) et la masse grasse (kg) ont été mesurées au niveau du corps entier à l'aide de l'absorption bi-photonique à rayons X (DXA). Le MetS a été défini selon les recommandations de la Fédération Internationale du Diabète. La concentration plasmatique en unOC a été déterminée par méthode immuno-enzymatique (ELISA). L'inflammation gingivale a été définie par la concentration de facteur de nécrose tumoral dans le fluide gingival créviculaire (GCF TNF-α) et par le niveau de saignement gingival. Résultats: Nous avons observé des associations positives entre la masse grasse et les mesures de santé osseuse indépendamment de la masse maigre. Plus précisément, une augmentation de 1-kg de masse grasse était associée respectivement avec une augmentation de 9,32 g (95% intervalle de confiance [IC]: 7,26 ; 11,39), 8,02 cm2 (95% IC: 6,72 ; 9,32) et 0,002 g/cm2 (95% IC: 0,000 ; 0,002), en BMC, surface osseuse et BMD.Les garçons présentant le MetS avaient une concentration en GCF TNF-α 49,5% (95% IC: 25,72 ; 73,22) plus élevée et 13,7% (95% IC: 1,1 ; 26,2) plus de sites de saignement gingival comparativement à ceux sans MetS. Par ailleurs, chez les garçons, pour 3 des 5 composantes du MetS - tour de taille, concentration plasmatique de triglycérides, pression artérielle systolique - une augmentation était associée à une concentration en GCF TNF-α plus élevée. Aucun de ces résultats n'a été observé chez les filles.Une augmentation de 1-ng/ml de la concentration plasmatique en unOC était associée à une diminution de 0.96% (95% IC: -1,69 ; -0,23) de la concentration en GCF TNF-α. Conclusion: Nos résultats montrent le regroupement de conditions médicales incluant des anomalies métaboliques, une faible concentration plasmatique en unOC et la présence d'inflammation gingivale chez des enfants de race blanche, âgés de 8-10 ans. Ces résultats suggèrent que le métabolisme des graisses ainsi que celui des os peuvent être associés à la santé parodontale à un jeune âge. Documenter l'association de ces conditions avec la santé parodontale chez l'enfant peut avoir des répercussions en santé publique. En effet, cela pourrait permettre d'identifier les personnes à risque de développer plusieurs conditions inter-reliées bien avant qu'elles ne se développent cliniquement et de mettre en place des mesures préventives.
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Pennington, S. R. "The effects of insulin on phosphoinositide metabolism in isolated fat cells". Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382660.
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Hodgson, Adrian. "Influence of nutritional interventions to optimise fat metabolism and exercise performance". Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4676/.
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This thesis investigated three commonly used nutritional interventions that are often claimed to alter substrate metabolism and improve exercise performance: green tea extract (GTE), coffee and vitamin D. GTE and caffeine have been hypothesized to increase fat oxidation at rest and during exercise, thereby lowering the reliance on skeletal muscle glycogen and improving endurance exercise capacity. We observed that 7 days GTE supplementation resulted in an increase in metabolites related to fat and energy metabolism at rest but not during moderate intensity exercise. The current thesis also found that endurance exercise performance can be improved to the same extent by either using coffee or caffeine. However, these improvements in endurance exercise performance were independent of changes to fat oxidation during exercise. We also demonstrate that athletes living in Birmingham, United Kingdom, display a high prevalence of vitamin D deficiency during the winter and thus require nutritional support. However, despite the high prevalence of vitamin D deficiency, there was no association between vitamin D status and skeletal muscle function or exercise performance. Short term vitamin D supplementation at doses above the current recommended daily allowance was highly effective in correcting vitamin D deficiency to sufficiency. But supplementation did not alter any measure of performance.
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Dunn, Sarah Louise Medical Sciences Faculty of Medicine UNSW. "Effects of exercise and dietary intervention on metabolic syndrome markers of inactive premenopausal women". Awarded by:University of New South Wales. Medical Sciences, 2009. http://handle.unsw.edu.au/1959.4/43914.
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The effects of exercise and dietary intervention on metabolic syndrome (Mets) markers of inactive premenopausal women were investigated. In Study I, early markers of MetS were examined in young, (21.2 ?? 0.3 years), healthy but unfit women (N = 66) consuming a processed food diet. A second aim was to examine the relationship between ethnic influences (European versus Chinese) and early markers of MetS (e.g., hyperinsulinemia). Study II compared the hormonal and metabolic responses to steady state exercise (SSE) and high intensity interval exercise (HIIE) in untrained young women (N = 18, 21.7 ?? 0.8 years). Women were further divided into high and low fasting insulin levels to determine if hyperinsulinemia influenced hormonal and metabolic response to SSE and HIIE. Study III examined the hormonal and metabolic response to a randomized controlled intervention named the Fish oil, Exercise and Mediterranean diet (FEM) trial. The FEM trial was conducted with overweight, inactive young (23.5 ?? 0.6 years) women (N = 56) for 12 weeks. Characteristics of a subset of women (N = 34, 23.5 ?? 0.7 years) in the FEM trial, non-responders (NRES), who did not lose weight (??? 1% loss in mass), were also examined. Metabolic profiles were developed based on body composition, aerobic fitness, blood markers, diet, resting metabolic rate, medical history, blood pressure, and autonomic function. Body composition was measured by skinfolds and girths, bioimpedance (Tanita, Japan), and Dual Energy X-Ray Absorptiometry. Peak oxygen uptake was assessed using an open circuit spirometer, TrueMax 2400 Metabolic Cart. Venepuncture and cannulation techniques were used for collecting blood samples that were also centrifuged and frozen for later analysis. In Study I young women who were physically unfit and consumed a processed food diet possessed high levels of fasting insulin, HOMA-IR (an insulin resistance index), and C-reactive protein (CRP). Insulin, p < .001, and HOMA-IR, p < .05, were significantly greater in Chinese Australians compared to European Australians, whereas plasma CRP levels were significantly, p < .05, lower. Significant differences, p < .05, existed between the groups with the Chinese Australians possessing lower body composition indices. However, ethnic differences still existed for insulin, HOMA-IR, and CRP after adjusting for body composition. Both groups consumed significantly high protein relative to their body mass. Thus, it appears that hyperinsulinemia is one of the earliest markers of MetS in young inactive females of both European and Asian descent who are unfit and consume a high level of dietary protein. In Study II, HIIE compared to SSE proved to be more effective at preventing an increase in insulin levels in the two hours after exercise. Resting respiratory quotient (RQ) was significantly lower, p < .05, following both HIIE and SSE, whereas plasma glycerol levels were higher, p = .06, suggesting greater lipolysis following HIIE. The women were divided by baseline fasting plasma insulin (> 9.98 ??IU/ml) into high insulin (HI) and low insulin groups (LI). The fasting plasma human growth hormone levels of the HI women were significantly lower at baseline compared to that of LI women. Baseline RQ was correlated with baseline glycerol, r = - .54, p < .05. Insulin levels at one hour post HIIE was related to fasting plasma adrenocorticotropic hormone (ACTH) one hour post exercise, r = .52, p < .05. Fasting plasma leptin at one, r = .56, p < .05, and two, r = .53, p < .05, hours post exercise was associated with 2 hour post insulin levels. Interestingly, fasting ACTH was significantly elevated in the 2 hours post exercise in the HI women compared to LI. All diet data between the groups were similar and lipids were in the healthy range with no significant differences between the women possessing high or low fasting plasma insulin. Thus, young women who completed one session of short duration HIIE compared to SSE improved certain aspects of their metabolic profile (e.g., reduced insulin levels) and enhanced their fat oxidation in the immediate two-hour exercise recovery period. Following FEM (a 12-week multi-component lifestyle intervention) overweight women recorded significantly lower, p < .05, body composition (mass, fat mass, percent body fat, waist circumference), insulin, inflammation (CRP), blood pressure, and lipids. The improvements within the Mediterranean diet (Mediet) were related to the reductions in body weight, fat mass, and insulin. Consumption of saturated fats, legumes, meat, poultry, and egg were also significantly decreased, p < .05, following the trial. Adherence to the Mediet and fish oil consumption, measured through a Mediet score, was significantly increased, p < .001, and was associated with reduced levels of fat mass, r = .43, p < .05. Autonomic function (measured by power frequency analysis), aerobic fitness, and fat oxidation were all significantly, p < .05, enhanced. Therefore, an intervention incorporating fish oil consumption, HIIE, and Mediet significantly reduced body fat, fasting insulin, inflammatory markers, and some blood lipids. Interestingly, some women did not lose fat mass following the FEM intervention, despite experiencing significant reductions in insulin, inflammation, waist circumference, blood pressure, and an increase in aerobic power. The major differences between those women who lost fat and those that did not was that the non-responders possessed significantly lower, p < .05, systolic blood pressure, lower resting heart rate, and a higher resting RQ. In summary, in Study I, young, unfit women consuming a processed diet, demonstrated hyperinsulinemia and low grade inflammation. The high levels of fasting insulin suggest that these women are at a higher risk for developing MetS and type 2 diabetes. The results of Study II suggests that one bout of HIIE compared to a longer bout of SSE was more effective at preventing a rise in post-exercise insulin levels. Finally, results of Study III indicate that a 12-week lifestyle intervention, encompassing HIIE, fish oil ingestion, and a Mediet positively influenced early MetS markers (e.g., hyperinsulinemia), aerobic and anaerobic fitness, low grade inflammation, and body composition in young women.
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Riggs, Amy Jo Gropper Sareen Annora Stepnick. "Changes in energy expenditure associated with injestion of high protein, high fat versus high protein, low fat meals among underweight, normal weight, and overweight females". Auburn, Ala., 2006. http://repo.lib.auburn.edu/2006%20Spring/doctoral/RIGGS_AMY_28.pdf.
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Ding, Min Judd Robert L. "Regulation of glucose metabolism in a hepatic and muscle cell line by adiponectin". Auburn, Ala., 2005. http://hdl.handle.net/10415/1263.
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Guardiola, Guionnet Montserrat. "Role of the apoa5 gene in lipid and fat-soluble vitamin metabolism". Doctoral thesis, Universitat Rovira i Virgili, 2008. http://hdl.handle.net/10803/8857.
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La malaltia cardiovascular és responsable d'un elevat nombre de morts en els països industrialitzats. La seva alta prevalença és deguda, principalment, a factors ambientals com l'estil de vida sedentari, el tipus de dieta rica en greixos i hàbits com el tabaquisme, que si s'afegeixen a una predisposició genètica pot resultar en un major risc de malaltia. Un dels factors determinants del desenvolupament de malaltia són els lípids, que en circulació són guiats per les apolipoproteïnes (APO). El mal funcionament d'aquestes proteïnes degut a variants genètiques pot influir, per exemple, en la quantitat de lípids i el temps que estiguin en circulació. L'APOA5 és clau en la modulació del metabolisme dels triglicèrids (TG) i la nostra hipòtesi és que l'APOA5 també pot modificar els nivells d'altres components del metabolisme altament lligats als TG, influint el procés de síntesi i secreció de partícules riques en TG.Utilitzant la variabilitat genètica de l'APOA5 en una població formada per homes sans i en una formada per pacients diabètics tipus 2, hem pogut descriure que els portadors de la variant -1131T>C presenten un augment de més del 15% en els nivells de TG, i que aquest efecte és principalment degut a un major contingut de TG en les partícules VLDL que trobem en circulació. També hem descrit que aquest variant afecta les concentracions de vitamina E en ambdues poblacions fent que augmentin els seus nivells circulants. Tot i que la vitamina E és un potent antioxidant, aquesta variant no afecta l'estat oxidatiu dels individus perquè els seus nivells augmenten en la mateixa mesura que ho fan els TG. Com que els nivells circulants de TG es poden veure influenciats per altres aspectes com el tractament farmacològic (p. ex. els inhibidors de la proteasa emprats pel tractament del la SIDA indueixen hipertrigliceridemia), vam estudiar el paper del gen en una població de pacients infectats pel virus VIH, i vam veure que en els individus tractats amb inhibidors de la proteasa, ser portador de la variant -1131T>C del gen APOA5 pot fer que els augmentin els nivells de TG més del 40%. També els augmenten els nivells de colesterol total en plasma, i això resulta en la presència d'un perfil lipídic pro-aterogènic.Per a aprofundir en els mecanismes d'acció de l'APOA5 hem utilitzat un model animal d'arteriosclerosi, el ratolí deficient en APOE. Disposàvem de diferents grups d'animals segons si rebien dieta convencional o rebien una dieta rica en greix saturat, suplementada o no amb colesterol, i els animals van ser sacrificats a diferents edats (16, 24 i 32 setmanes). Hem descobert que l'expressió del gen APOA5 en fetge es troba reprimida pel greix saturat de la dieta, arribant a disminuir fins un 75%. A més, l'expressió del gen en fetge augmenta significativament amb l'edat dels animals. També hem publicat que l'expressió hepàtica d'APOA5 correlaciona amb l'àrea de la lesió arterioscleròtica i el grau d'inflamació en aquests animals.Fins ara es creia que el gen només s'expressava en fetge. El fetge és un dels principals òrgans reguladors del metabolisme lipídic i és el responsable de la síntesi de partícules riques en TG d'origen endogen, però no és l'únic. L'intestí també s'encarrega de sintetitzar partícules riques en TG d'origen exogen. En aquest treball també hem demostrat que el gen APOA5 no s'expressa únicament en fetge en humans, sinó que també es troba en intestí. Per a dur a terme aquests experiments, vam utilitzar un model cel·lular d'intestí humà (cèl·lules TC7/ Caco2), i tot i que s'expressa a baixos nivells, hem pogut descriure que la seva expressió a l'intestí es veu modulada per components de la dieta (àcids grassos de cadena llarga i de cadena curta) i fàrmacs hipolipemiants (agonista PPARα).Conclusió: l'APOA5 és un gen clau modulant els nivells circulants de TG, tant en homes sans com en pacients dislipèmics (diabètics o pacients VIH sota tractament antiretroviral), i la seva expressió es veu alterada per components de la dieta, tant en fetge com en intestí, i per fàrmacs hipolipemiants.
Cardiovascular disease is the main cause of mortality in industrialised countries. Its high prevalence is mainly due to environmental factors (sedentary lifestyle, saturated fat rich diet and tobacco consumption, among others), which together with genetic predisposition could result in increased disease risk. One of the key factors in the development of atherosclerosis are circulating lipids which are guided by the apolipoproteins (APO). The malfunctioning of these proteins due to genetic variants could affect, for example, the concentration and circulating time of lipids. The APOA5 is a key gene modulating triglyceride (TG) metabolism, and our hypothesis is that APOA5 may also modify the circulating levels of other metabolic components highly linked to TG by influencing the synthesis and secretion of TG-rich particles.
Using the genetic variability of the APOA5 gene in two populations, healthy men and type 2 diabetic patients, we have described that carriers of the -1131T>C variant present with more than 15% higher TG levels, being this effect mainly due to a greater TG content in circulating VLDL particles. We have also described that this variant affects vitamin E concentrations in both populations, increasing its levels in circulation. Vitamin E is a potent antioxidant, but this variant does not affect the oxidative status of the subjects, because its levels rise in the same proportion than TG do.Since the circulating TG levels can be affected by other factors such as the pharmacological treatment (for example, the protease inhibitors used for the AIDS therapy induce hypertriglyceridemia), we studied the role of APOA5 in a population of patients infected by the VIH virus, and we found that in the group of subjects treated with protease inhibitors, carrying the -1131C variant could increase more than 40% the levels of circulating TG. They also present with increased plasma total cholesterol levels, resulting in the presence of a pro-atherogenic lipid profile.
To go deeper in the mechanisms of APOA5 we have used an animal model for atherosclerosis, the APOE-deficient mouse. We had different groups of animals depending on whether they received conventional diet or a saturated fat rich diet supplemented or not with cholesterol. The animals were sacrificed at different ages (16, 24 and 32 weeks). We have demonstrated that the hepatic expression of the APOA5 gene is repressed by dietary saturated fat, reaching a 75% descent. Furthermore, the hepatic expression of APOA5 increases with the age of the animals. We have also published that the expression of APOA5 correlates with the atherosclerotic lesion area and the degree of inflammation in those animals. Till date, it has been published that the gene was only expressed in the liver. The liver is one of the main organs regulating lipid metabolism and is responsible of the synthesis of particles rich in TG from an endogenous origin, but is not the only tissue capable of doing that. The intestine is also involved in the synthesis of TG-rich particles from exogenous origin. We have also demonstrated that APOA5 is not only expressed in the liver in humans, but also in the intestine. For that purpose we used a human intestine cell model (TC-7/ Caco2 cells), and although it is expressed at low levels, we have been able to describe that its intestinal expression is modified by dietary components (long- and short-chain fatty acids) and by hypolipemiant drugs (a PPARα agonist).
Conclusion: APOA5 is a key gene modulating circulating TG levels, in dislipemic patients (diabetics or HIV patients under antiretroviral treatment) and even in healthy men, and its expression is affected by dietary components, in the liver and in the intestine, and also by hypolipemiant drugs.
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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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Souza, Paulo Fernando Araujo de. "The effects of dietary fat on the metabolism of the lactating rat". Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276817.
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Oakley, Francesca Rachel. "The influence on dietary fat on plasma lipoprotein metabolism and haemostatic variables". Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314045.
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Eaves, Audrey Denise Houmard Joseph A. "Effects of parental obesity on fat metabolism during submaximal exercise in children". [Greenville, N.C.] : East Carolina University, 2009. http://hdl.handle.net/10342/1905.
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Thesis (M.S.)--East Carolina University, 2009.Presented to the faculty of the Department of Exercise and Sport Science. Advisor: Joseph Houmard. Title from PDF t.p. (viewed May 4, 2010). Includes bibliographical references.
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Hayes, Jasmine Marie. "Skeletal Muscle Adaption to 5 days of High-Fat Feeding in Humans". Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/85059.
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Skeletal muscle is highly involved in macronutrient metabolism. To maintain proper energy metabolism and physiology, skeletal muscle must adapt to nutrient supply. Thus, diet macronutrient composition is an important modulator of skeletal muscle metabolism. Evidence from rodent and human models show high-fat diets contribute to impaired insulin signaling, as well as decreased fatty acid and glucose oxidation. Utilizing proteomic analysis of metabolic proteins in humans may lead to the mechanism behind skeletal muscle adaption to macronutrient composition, potentially providing the groundwork for characterizing the etiology of high-fat feeding induced metabolic disease. The objective of this study was to compare the substrate oxidation patterns and the levels of metabolic proteins in the fasted skeletal muscle of lean, healthy males that either increased fatty acid oxidation in response to the high-fat diet, termed responders, or males that decreased fatty acid oxidation, termed non-responders. We employed a controlled feeding study design, where the participants served as their own controls. Following a 2-week control diet (30% fat, 55% carbohydrate and 15% protein), participants came to the lab fasted overnight and a muscle biopsy was taken from their vastus lateralis muscle. Participants were then placed on a 5-day high-fat diet (50% fat [45% saturated fat], 35% carbohydrate, and 15% protein). Following this diet, participants again came to the lab fasted overnight and another muscle biopsy was taken from their vastus lateralis muscle. Both the control and the high-fat diets were isocaloric to habitual diets. Muscle from the biopsies were utilized for substrate metabolism measures and mass spectrometry. We did not observe any significant differences in glucose oxidation between responders and non-responders, prior to or following the high-fat diet. Our proteomic analysis identified 81 proteins and protein subunits involved in substrate metabolism but only 6 were differentially regulated by the high-fat diet. Independent of the high-fat diet, compared to non-responders, responders contained an overall higher content of protein subunits belonging to Complex I and ATP synthase. The findings from this study suggest that adaption to high-fat feeding is individual specific and proteomic changes alone cannot explain high-fat feeding induced metabolic changes.Ph. D.
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Tang, Ling. "The effect of pharmacological and dietary modulators of lipid metabolism on gene expression in a porcine model". Auburn, Ala., 2006. http://repo.lib.auburn.edu/2006%20Summer/Dissertations/TANG_LING_28.pdf.
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Dinis, Ana Paula Gonçalves. "Níveis plasmáticos de lipídios em ratos submetidos à dieta com gordura suína como fonte lipídica após esplenectomia total isolada ou combinada com implante esplênico autógeno". Universidade do Estado do Rio de Janeiro, 2008. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2053.
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Alguns estudos experimentais têm sugerido um importante papel do baço no metabolismo lipídico. Poucas análises, entretanto, avaliam o impacto que diferentes fontes de gordura possam exercer sobre os níveis de lipídios plasmáticos. O objetivo deste trabalho foi analisar o efeito de uma dieta nutricionalmente equilibrada (NE) e de uma dieta com gordura suína (GS) como fonte lipídica nos níveis de lipídios plasmáticos em ratos submetidos a esplenectomia total (ET) isolada ou combinada com implante esplênico autógeno (IEA). Foram utilizados 60 ratos Wistar machos adultos, distribuídos em seis grupos, cada um com dez animais: Grupo 1 controle operação simulada, com oferta de ração NE; Grupo 2 controle operação simulada, com oferta de ração GS; Grupo 3 submetidos a ET, com oferta de ração NE; Grupo 4 submetidos a ET, com oferta de ração GS; Grupo 5 submetidos a ET combinada com IEA e com oferta de ração NE; e Grupo 6 submetidos a ET combinada com IEA e com oferta de ração GS. Foram coletadas amostras sangüíneas imediatamente antes da operação (D0), e após 12 semanas de experimento (D+12), para verificação do perfil lipídico, quando os animais foram mortos, com retirada dos implantes esplênicos nos grupos 5 e 6. Houve regeneração morfológica de todos os tecidos esplênicos implantados, não se observando diferença no percentual de regeneração entre os grupos 5 e 6. Não houve diferença no ganho de peso e no consumo de ração entre os grupos de animais, assim como no lipidograma dos animais alimentados com dieta NE quando comparados os níveis plasmáticos em D0 e em D+12, enquanto nos grupos com modificação da fonte lipídica houve elevação das concentrações de colesterol total (CT), lipoproteína de baixa densidade (LDL), lipoproteína de muito baixa densidade (VLDL), triglicerídeos (TGL) e diminuição da concentração de lipoproteína de alta densidade (HDL). Quando comparados os seis grupos de animais, em D+12, apenas os níveis plasmáticos de HDL dos animais dos grupos 2, 4 e 6 apresentaram-se significativamente menores que os do grupo 3. Os resultados deste estudo permitem concluir que a dieta nutricionalmente equilibrada mantém os níveis de lipídios plasmáticos, enquanto a dieta à base de gordura suína provoca alterações no perfil lipídico de ratos alimentados com este tipo de ração, independentemente do procedimento cirúrgico realizado sobre o baço.An important role of the spleen in lipid metabolism has been suggested by clinical and experimental studies. Few studies, however, have evaluated the impact of different sources of fat in plasma lipid levels. The purpose of the present investigation was to analyze the effect of a nutritionally balanced (NB) diet and a diet containing pork fat (PF) as sources of lipids on the lipid profile of rats submitted to total splenectomy (TS) alone or combined with splenic autotransplantation (SA). Sixty adult male Wistar rats were divided into six groups of 10 animals each: Group 1 sham-operated, fed the NB diet; Group 2 sham-operated, fed the PF diet; Group 3 TS, fed the NB diet; Group 4 TS, fed the PF diet; Group 5 SA, fed the NB diet; and Group 6 SA, fed the PF diet. Blood samples were collected immediately before the operation (D0) and 12 weeks after the beginning of the experiment (D+12) for plasma lipid determination. On D+12, the animals were killed and the splenic implants of groups 5 and 6 were removed. Morphologic regeneration of splenic tissues was observed, with no difference in percent regeneration between these two groups. Weight gain and chow intake were similar among all groups of animals. When D+12 plasma lipid levels were compared to D0, there were no differences in groups 1, 3, and 5, while in groups 2, 4, and 6 total cholesterol (TC), low density lipoprotein (LDL), very low density lipoprotein (VLDL), and triglycerides (TGL) levels had increased and high density lipoprotein (HDL) levels had decreased. At the end of the experiment, only the HDL levels of groups 2, 4, and 6 were lower than group 3 levels. Our results lead us to conclude that, regardless of the surgical spleen procedure to which the rats were submitted, a nutritionally balanced diet maintained plasma lipid levels, while a diet containing pork fat as a source of lipids led to alterations in lipid profile.
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Zubia, Raul Y. "Substrate oxidation and energy expenditure during and one hour after isocaloric exercise bouts of different intensity". To access this resource online via ProQuest Dissertations and Theses @ UTEP, 2008. http://0-proquest.umi.com.lib.utep.edu/login?COPT=REJTPTU0YmImSU5UPTAmVkVSPTI=&clientId=2515.
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Burén, Jonas. "Glucose and lipid metabolism in insulin resistance : an experimental study in fat cells". Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-26.
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Type 2 diabetes is usually caused by a combination of pancreatic β-cell failure and insulin resistance in target tissues like liver, muscle and fat. Insulin resistance is characterised by an impaired effect of insulin to reduce hepatic glucose production and to promote glucose uptake in peripheral tissues. The focus of this study was to further elucidate cellular mechanisms for insulin resistance that may be of relevance for type 2 diabetes in humans. We used rat and human adipocytes as an established model of insulin’s target cells. Glucocorticoids, e.g. cortisol, can induce insulin resistance in vivo. In the present study, pretreatment of rat adipocytes in vitro for 24 h with the cortisol analogue dexamethasone produced a downregulation of glucose uptake capacity as well as a marked depletion of cellular insulin receptor substrate 1 (IRS-1) and protein kinase B (PKB), two proteins suggested to play a critical role in the intracellular signal transduction pathway of insulin. The amount of phosphorylated PKB in response to acute insulin treatment was decreased in parallel to total PKB content. The basal rate of lipolysis was enhanced, but insulin’s antilipolytic effect was not consistently altered following dexamethasone pretreatment. Alterations in blood glucose as well as insulin levels may be of great importance for cellular as well as whole-body insulin resistance. High glucose (≥15 mM) for 24 h induced a decrease in glucose uptake capacity in rat adipocytes and IRS-1 content was reduced whereas IRS-2 was increased. Long-term pretreatment with a high insulin concentration downregulated insulin binding capacity and when combined with high glucose, it produced a pronounced reduction of cellular IRS-1 and 2 content together with insensitivity to insulin’s effect to activate PKB and a decrease in glucose uptake capacity. A common denominator for a decrease in glucose uptake capacity in our rat adipocyte studies seems to be a decrease in IRS-1 content. Adipocytes from type 2 diabetes patients are insulin-resistant, but in our work the insulin resistance could be reversed by incubation of the cells at a physiological glucose level for 24 h. Insulin resistance in fresh adipocytes from type 2 diabetes patients was associated with in vivo insulin resistance and glycemic level and with adipocyte cell size and waist-hip ratio (WHR). As a potential mechanism for postprandial dyslipidemia in type 2 diabetes, we examined the nutritional regulation of subcutaneous adipose tissue lipoprotein lipase (LPL) activity. It was upregulated by ~40-50 % after a standardised lipid-enriched meal and this was very similar in type 2 diabetes patients and control subjects, suggesting that the postprandial hypertriglyceridemia found in type 2 diabetes is not explained by an altered nutritional regulation of LPL in subcutaneous fat. In conclusion, the present work provides evidence for novel interactions between glucocorticoids and insulin in the regulation of glucose metabolism that may potentially contribute to the development of insulin resistance. High levels of glucose and insulin produce perturbations in the insulin signalling pathway that may be of relevance for human type 2 diabetes. Cellular insulin resistance may be secondary to the diabetic state in vivo, e.g. via glucotoxicity. This is supported by our finding that insulin resistance in adipocytes from type 2 diabetes patients can be reversed after incubation at a physiological glucose level. Key words: adipocyte, insulin resistance, type 2 diabetes, insulin signalling, glucose uptake, insulin, glucose, dexamethasone, insulin receptor substrate, protein kinase B, GLUT4, lipoprotein lipase.
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Zhou, Xun. "LMO4 is Required for Central Leptin Control of Fat Metabolism and Insulin Sensitivity". Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19948.
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Metabolic homeostasis is orchestrated by the hypothalamus through the neuroendocrine and the autonomic nervous systems. The hypothalamic nuclei respond to the peptide leptin secreted from adipose tissue to suppress feeding and increase energy expenditure by promoting fat metabolism via sympathetic activity. Another important, but perhaps less appreciated function of central leptin signaling is to elevate peripheral insulin sensitivity. Environmental and genetic risk factors that affect hypothalamic leptin signaling can lead to obesity and type 2 diabetes mellitus (T2DM).
Here, we discovered that LIM domain only 4, LMO4, is a novel protein participating in central leptin signaling. In a process strikingly similar to T2DM in humans, CaMKIIα-Cre;LMO4flox/flox mice, which have LMO4 knocked out in the postnatal brain including the hypothalamus, develop visceral adiposity, reduced insulin sensitivity, obesity and diabetes when fed with regular chow. Central leptin signaling was significantly lost in key hypothalamic nuclei of mutant mice. Caloric restriction prevents obesity but not insulin resistance in these mice. Taken together, our results suggest that LMO4 function in the brain is required for central leptin signaling to control fat metabolism and peripheral insulin sensitivity.
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Faraj, May. "Postprandial plasma acylation stimulating protein reponse and fat metabolism in post-obese women". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0015/MQ55054.pdf.
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Pitsiladis, Yannis P. "Diet manipulation, altered fat and carbohydrate metabolism and exercise performance in trained humans". Thesis, University of Aberdeen, 1996. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU089995.
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The aim of the first two experiments was to determine whether alterations in dietary carbohydrate (CHO) intake would affect performance of high intensity exercise in well-trained individuals. This was achieved by comparing the effects of a 70 and 40% CHO diet on the performance of high intensity exercise lasting approximately 10 min (Experiment 1) or 30 min (Experiment 2). At both exercise intensities, no difference in exercise performance was found. These results demonstrated that moderate changes in diet composition during normal training do not significantly affect performance of high intensity exercise in well-trained individuals. These findings would suggest that total muscle glycogen concentration was not limiting high intensity exercise performance. The higher than normal daily energy intake of the subjects' diet may have adequately compensated for the reduced percentage of CHO on the two low CHO diets. An increased fat oxidation on the low CHO trial may also have contributed to these results. These results do not exclude the possibility that the glycogen content of individual muscle fibres was limiting high intensity exercise performance. The aim of the third experiment was to determine the effects of an exercise and diet regime, which was intended to alter initial muscle glycogen concentration, on the capacity of well-trained individuals to perform prolonged strenuous exercise to exhaustion in the heat and the cold. Exercise capacity in the heat was reduced compared with exercise in the cold, irrespective of diet. The exercise and diet intervention, when aimed at increasing muscle CHO stores, improved exercise capacity both in the heat and in the cold compared with when the intervention was aimed to reducing CHO stores.
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Cha, Ming Chuan 1955. "Effects of dietary fat selection and energy restriction on tissue lipid metabolism : structure, function and regulation". Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35684.
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To investigate interactive effects of dietary fatty acid composition and energy restriction on body lipid metabolism and its regulation, rats were fed for 10 weeks diets varying in fat type and energy intake level. Energy deficiency was achieved by removing carbohydrate from the diets while keeping fat and other nutrient intakes constant. Tissue fatty acid deposition was influenced by the interaction between the dietary fat source and body energy balance. Less total fatty acids were deposited in livers of the ad libitum beef tallow-fed animals than the other fat feedings. However, such difference no longer existed when energy intake was restricted. Similarly, less energy supply eliminated the higher docosahexaenoic acid and lower arachidonic acid contents associated with the fish oil feeding in hepatocyte membrane phosphatidylchohne, phosphatidylserine and sphingomyelin. Tissue lipogenesis was also examined as a function of the interaction of dietary fatty acid composition and energy restriction. Comparable absolute cholesterol synthesis rates were observed in livers of the food restricted animals fed different types of dietary fat, although the synthesis rates were different among the dietary fat groups fed ad libitum. Energy restriction increased the triglyceride-fatty acid synthesis rates in the intestine of the fish and safflower oil-fed groups, but not in that of the olive oil- and beef tallow-fed animals. Plasma leptin concentrations were 60% higher in the ad libitum-fed fish and safflower oil groups as compared with those in the beef tallow diet group, despite smaller perirenal fat mass and fat cell size in the fish oil-fed animals. Energy restriction decreased plasma leptin levels of the fish and safflower oil-fed rats, but not those in the beef tallow-fed animals. Taken together, these results demonstrate that the structural, functional and regulating aspects of tissue lipid metabolism were influenced by an interaction between dietary fatty acid composit
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Wee, Shiou-Liang. "Influence of the type of carbohydrate breakfasts on metabolism and endurance running capacity in man". Thesis, Loughborough University, 1999. https://dspace.lboro.ac.uk/2134/13775.
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Compared to the overnight fasted state, a high carbohydrate (CHO) breakfast 3-4 hours before exercise enhances endurance performance. However, the optimal type or composition of the pre-exercise meal to be consumed is less clear. Glycaemic and insulinaemic responses to a meal play a key role in subsequent metabolism during exercise. The investigations described in this thesis focused on the influence of I) the composition and 2) glycaemic index (GI) of CHO breakfasts 3 hours before exercise on postprandial and exercise metabolism and endurance running capacity.
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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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Stephens, Brooke R. "The influence of biological maturation on fat and carbohydrate metabolism during exercise in boys". Virtual Press, 2003. http://liblink.bsu.edu/uhtbin/catkey/1260630.
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The purpose of this study was to examine the influence of biological maturation on the pattern of fat and carbohydrate metabolism during exercise in early-pubertal (EP), mid-pubertal (MP), and late-pubertal (LP) males. Nine boys, Tanner stage I (EP) (10.3 ±0.9 years), 12 boys, Tanner stage 2/3 (MP) (12.3 ± 1.9 years), and 11 boys, Tanner stage 4/5 (LP) (15.0 ± 0.8 years) were subjects. Maximal aerobic capacity (VO2max) was assessed and, on a separate day, 5, 5-minute exercise bouts on a cycle ergometer at 30, 40, 50, 60, and 70% Of VO2max were performed in a fasted state. Fuel use was calculated at each intensity using steady-state V02 and the respiratory exchange ratio (RER). A one-way ANOVA was used to analyze physical characteristics and maximal exercise responses between groups. A two-way (group x intensity) ANOVA was used to analyze responses during submaximal exercise. Statistical significance was set at p < 0.05. VO2max (ml•kg-l.min 1) was not different between groups. At each intensity, % VO2ma., was similar between groups (p > 0.05). Significant interactions were found for RER, carbohydrate utilization, % fat utilization, and lactate concentration. Post hoc analyses revealed that at all intensities, % fat use and fat oxidation rates were higher and carbohydrate use and carbohydrate oxidation rates were lower in MP versus LP. In comparison, between EP and LP, % fat use was higher and % carbohydrate use was lower at 50-60% of VO2max, while fat oxidation rate was higher in EP versus LP at 40, 50, and 60% of VO2max. The only differences between EP and MP were for % fat and carbohydrate use at 30% of VO2max. Lactate concentrations were also lower in EP and MP than in LP at intensities corresponding to 50, 60, and 70% of VO2m., while no differences were observed between EP and MP at any intensity. The lack of a significant difference in substrate utilization or lactate concentrations between EP and MP at the majority of exercise intensities, suggest that the development of an adult-like metabolic profile occurs in the transition from mid-puberty to late-puberty.School of Physical Education