Regulation of Lipolysis in Adipocytes

Duncan, Robin E.; Ahmadian, Maryam; Jaworski, Kathy; Sarkadi-Nagy, Eszter; Sul, Hei Sook

doi:10.1146/annurev.nutr.27.061406.093734

Cited by 812 publications

(751 citation statements)

References 152 publications

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“…23 In contrast, HSL and ATGL are the key enzymes catalyzing the lipolysis of triacylglycerol in adipose tissue and its high activity attenuates triglyceride accumulation in adipocytes. 24 High-fat diets have been shown to elevate PPARg expression, leading in adipose tissues to an increase in lipogenic gene expression. 19 Therefore, after ingesting oil consisting of different P/S ratios and MUFA percentages, it is essential to determine whether obese animals fed a low-fat diet feature fat accumulation and obesity control changes related to modifications in adipocyte-derived hormones (leptin and adiponectin), adipocyte-derived enzymes (LPL and HSL) and adipocyte-specific gene (PPARg) expressions.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of high MUFA with high or low P/S ratio (polyunsaturated to saturated fatty acids) on improving hepatic lipolytic enzymes and mediating PPARγ related with lipoprotein lipase and hormone-sensitive lipase of white adipose tissue in diet-induced obese hamster

Liou

et al. 2010

Int J Obes

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Objective: The aim of this study was to assess the relationship between high monounsaturated fatty acids (MUFAs) with different levels of polyunsaturated-to-saturated fatty acid (P/S) ratios and body fat loss in diet-induced obesity (DIO) models. Design: Male Golden Syrian hamsters were randomly assigned to the control group (n ¼ 12) and obesity group (n ¼ 24) for 4 weeks of the high-fat DIO period; afterward, six hamsters from each group were killed. The remaining control hamsters were still fed a low-fat diet. For an additional 8 weeks, the remaining obesity hamsters were switched to a low-fat diet and subdivided into three subgroups (n ¼ 6/group): the obesity-control (ObC) group, high MUFA with high P/S ratio oil (HMHR) group and olive oil (OO) group. Serum insulin and leptin concentrations were measured, and hepatic fatty acid metabolic enzymes and adipose differentiation markers were determined using enzyme activities analysis, western blot and semiquantification reverse-transcription PCR. Results: No difference was observed in the mean energy intake through all study periods. After the DIO period, the obesity group increased in weight gain and epididymal fat weight compared with the control group. DIO hamsters in the HMLR group had significant reductions in white adipose tissue deposition and plasma leptin levels, suppression in adipose peroxisome proliferator-activated receptor-g (PPARg) and lipoprotein lipase (LPL) mRNA expressions and increases in hepatic acyl-CoA oxidase and carnitine palmitoyltransferase-I activities and mRNA levels compared with those in the ObC group. The HMHR group had upregulated phosphorylation of hormone-sensitive lipase (HSL) relative to total HSL protein levels compared with the OO group. However, the OO group had significantly elevated hepatic de novo lipogenesis compared with the HMHR group. Conclusions: HMHR seemed to be beneficial in depleting white adipose tissue accumulation by decreasing adipose PPARg and LPL mRNA expressions and mediating phosphorylation of HSL, and by improving hepatic lipolytic enzyme activities and mRNA expressions involved in b-oxidation in DIO hamsters.

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Section: Introductionmentioning

confidence: 99%

Differential effects of high MUFA with high or low P/S ratio (polyunsaturated to saturated fatty acids) on improving hepatic lipolytic enzymes and mediating PPARγ related with lipoprotein lipase and hormone-sensitive lipase of white adipose tissue in diet-induced obese hamster

Liou

et al. 2010

Int J Obes

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“…FFA levels are normally at their highest in the fasting state and go down in the postprandial state due to the suppressive action of insulin on lipolysis [31][32][33] . Here we found hepatic miR-378 expression is regulated by FFA, while insulin treatment in fasted mice could reduce the expression of miR-378.…”

Section: Discussionmentioning

confidence: 99%

Hepatic miR-378 targets p110α and controls glucose and lipid homeostasis by modulating hepatic insulin signalling

et al. 2014

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Understanding the regulation of insulin signalling in tissues provides insights into carbohydrate and lipid metabolism in physiology and disease. Here we show that hepatic miR-378/378* expression changes in response to fasting and refeeding in mice. Mice overexpressing hepatic miR-378/378* exhibit pure hepatic insulin resistance. miR-378 inhibits hepatic insulin signalling through targeting p110a, a subunit of PI3K and hence a critical component of insulin signalling. Knockdown of hepatic p110a mimics the effect of miR-378, while restoration of p110a expression abolishes the action of miR-378 on insulin signalling as well as its systemic effects on glucose and lipid homeostasis. miR-378/378* knockout mice display hypoglycemia and increased hepatic triglyceride level with enhanced insulin sensitivity. Inhibition of hepatic p110a in miR-378/378* knockout mice corrects the abnormal glucose tolerance. Finally, we show that overexpression of hepatic miR-378/378* ameliorates hepatic steatosis in ob/ob mice without exacerbating hyperglycemia. Our findings establish fasting-responsive miR-378 as a critical regulator of hepatic insulin signalling.

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“…Although they are constantly turned over by lipolysis and re-esterification, their mobilization and storage are precisely balanced by various hormones and other factors depending on the nutritional state (2). The net rate of lipolysis is increased during fasting or periods of increased energy demand.…”

Section: Gpr109b Is Coupled To G I -Type G-proteins and Is Activatedmentioning

confidence: 99%

Deorphanization of GPR109B as a Receptor for the β-Oxidation Intermediate 3-OH-octanoic Acid and Its Role in the Regulation of Lipolysis

Ahmed

Tunaru

Langhans

et al. 2009

Journal of Biological Chemistry

103

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The orphan G-protein-coupled receptor GPR109B is the result of a recent gene duplication of the nicotinic acid and ketone body receptor GPR109A being found in humans but not in rodents. Like GPR109A, GPR109B is predominantly expressed in adipocytes and is supposed to mediate antilipolytic effects. Here we show that GPR109B serves as a receptor for the ␤-oxidation intermediate 3-OH-octanoic acid, which has antilipolytic activity on human but not on murine adipocytes. GPR109B is coupled to G i -type G-proteins and is activated by 2-and 3-OH-octanoic acid with EC 50 values of about 4 and 8 M, respectively. Interestingly, 3-OH-octanoic acid plasma concentrations reach micromolar concentrations under conditions of increased ␤-oxidation rates, like in diabetic ketoacidosis or under a ketogenic diet. These data suggest that the ligand receptor pair 3-OH-octanoic acid/GPR109B mediates in humans a negative feedback regulation of adipocyte lipolysis to counteract prolipolytic influences under conditions of physiological or pathological increases in ␤-oxidation rates.

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Regulation of Lipolysis in Adipocytes

Cited by 812 publications

References 152 publications

Differential effects of high MUFA with high or low P/S ratio (polyunsaturated to saturated fatty acids) on improving hepatic lipolytic enzymes and mediating PPARγ related with lipoprotein lipase and hormone-sensitive lipase of white adipose tissue in diet-induced obese hamster

Differential effects of high MUFA with high or low P/S ratio (polyunsaturated to saturated fatty acids) on improving hepatic lipolytic enzymes and mediating PPARγ related with lipoprotein lipase and hormone-sensitive lipase of white adipose tissue in diet-induced obese hamster

Hepatic miR-378 targets p110α and controls glucose and lipid homeostasis by modulating hepatic insulin signalling

Deorphanization of GPR109B as a Receptor for the β-Oxidation Intermediate 3-OH-octanoic Acid and Its Role in the Regulation of Lipolysis

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