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offspring of rats exposed to BPA fed on a HFD compared with controls fed on a HFD. Figure 2 The effect of BPA on hepatic energy metabolism in the liver. (A) mRNA expression of genes associated with lipogenesis, fatty acid oxidation, and gluconeogenesis. (B
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unexplored. The liver plays a key role in whole-body energy homeostasis by regulating lipogenesis and fatty acid oxidation ( Reddy & Rao 2006 ). A large body of evidence has shown that two transcription factors, sterol regulatory element-binding protein 1c
Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
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Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
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Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
Cardiac Electrophysiology Research and Training Center, Cardiac Electrophysiology Unit, Center of Excellence in Cardiac Electrophysiology Research, Department of Oral Biology and Diagnostic Sciences, Faculty of Medicine
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level ( Nishimura et al . 2000 ) and fatty acid β oxidation (FAO) which is the primary energy source for the myocardium ( Vega et al . 2000 , Planavila et al . 2013 ). Under stress conditions, FGF21 has been shown to reduce the apoptosis of Islet β
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contribute to hepatic lipogenesis, VLDL-triglyceride (TG) and VLDL-cholesterol secretion, fatty acid (FA) oxidation and increased serum cholesterol levels (Zarjevski et al. 1993, Stafford et al. 2008, Zhang et al. 2010, Bruinstroop et al. 2012, Xie
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status between the mouse and hamster adrenals, we evaluated the expression of a few core genes involved in the regulation of these processes. We found that Cpt1a , a transferase essential for mitochondrial fatty acid oxidation (FAO), was substantially
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Leptin directly increases the rate of exogenous glucose and fatty acids oxidation in isolated adipocytes. However, the effects of leptin on fatty acid metabolism in white adipose tIssue have not been examined in detail. Here, we report that in adipocytes incubated for 6 h in the presence of leptin (10 ng/ml), the insulin-stimulated de novo fatty acid synthesis was inhibited by 36% (P<0.05), while the exogenous oxidation of acetic and oleic acids was increased by 50% and 76% respectively. Interestingly, leptin did not alter the oxidation of intracellular fatty acids. Leptin-incubated cells presented a 16-fold increase in the incorporation of oleic acid into triglyceride (TG) and a 123% increase in the intracellular TG hydrolysis (as measured by free fatty acids release). Fatty acid-TG cycling was not affected by leptin. By employing fatty acids radiolabeled with (3)H and (14)C, we could determine the concomitant influx of fatty acids (incorporation of fatty acids into TG) and efflux of fatty acids (intracellular fatty acids oxidation and free fatty acids release) in the incubated cells. Leptin increased by 30% the net efflux of fatty acids from adipocytes. We conclude that leptin directly inhibits de novo synthesis of fatty acids and increases the release and oxidation of fatty acids in isolated rat adipocytes. These direct energy-dissipating effects of leptin may play an important role in reducing accumulation of fatty acids into TG of rat adipose cells.
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an enzyme present in the outer mitochondria membrane that regulates β-oxidation by transferring long-chain fatty acids into the mitochondria ( Schreurs et al. 2010 ). Therefore, we postulated that the anti-adipogenic effect of LA was partially
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-shortened fatty acids to the mitochondria for complete oxidation, was significantly higher in leptin compared with pair-fed rats ( Fig. 4B ). As a result, the contribution of peroxisomes to the complete plamitate oxidation was increased from 39% in pair-fed to 63
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Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
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Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
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Introduction Obesity is associated with elevated circulating free fatty acids (FFAs) and FFAs cause insulin resistance ( Lewis et al . 2002 , Xiao et al . 2008 ). FFAs induce oxidative stress ( Nakamura et al . 2009 , Yuzefovych et al . 2010
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timepoints 0, 5, 10, 15, 30, and 60 min after the 6 h fasting period, then cell lysates were collected for immunoblotting analyses. Biochemical analysis Fatty acid oxidation (FAO) enzyme activity was measured in livers of HFHS-fed mice using a