scholarly journals Fasting, But Not Exercise, Increases Adipose Triglyceride Lipase (ATGL) Protein and Reduces G(0)/G(1) Switch Gene 2 (G0S2) Protein and mRNA Content in Human Adipose Tissue

2011 ◽  
Vol 96 (8) ◽  
pp. E1293-E1297 ◽  
Author(s):  
Thomas S. Nielsen ◽  
Mikkel H. Vendelbo ◽  
Niels Jessen ◽  
Steen B. Pedersen ◽  
Jens O. Jørgensen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Research Unit ◽  
Hormone Sensitive Lipase ◽  
University Hospital ◽  
Adipose Triglyceride Lipase ◽  
Triglyceride Lipase ◽  
Protein Levels ◽  
Mrna Content ◽  
Underlying Mechanisms

Abstract Context: Fasting and exercise are characterized by increased lipolysis, but the underlying mechanisms are not fully understood. Objective: The study was designed to test whether fasting and exercise affect mRNA and protein levels of adipose triglyceride lipase (ATGL) and G(0)/G(1) switch gene 2 (G0S2), a recently discovered ATGL inhibitor, in humans. Design and Participants: We studied eight healthy men (age, 25.5 ± 4.3 yr) for 6 h (a 4-h basal and a 2-h clamp period) on three occasions in a randomized crossover design: 1) in the basal state and after; 2) 72-h fasting; and 3) 1-h exercise (65% VO2max). Subcutaneous abdominal adipose tissue (AT) biopsies were taken at t = 30 and 270 min. Setting: The study was conducted at a university hospital research unit. Results: Circulating free fatty acids and GH were increased, and C-peptide was decreased by both fasting and exercise. During fasting, insulin failed to suppress free fatty acid levels, suggesting AT insulin resistance. ATGL protein was increased 44% (P < 0.001), and G0S2 mRNA and protein were decreased 56% (P = 0.02) and 54% (P = 0.01), respectively, after fasting, but both ATGL and G0S2 were unaffected by exercise. Protein levels of hormone-sensitive lipase and comparative gene identification-58 were unaffected throughout. Conclusions: We found increased AT content of ATGL and decreased protein and mRNA content of the ATGL inhibitor G0S2, suggesting increased ATGL activity during fasting, but not after short-term exercise. These findings are compatible with the notion that the ATGL-G0S2 complex is an important long-term regulator of lipolysis under physiological conditions such as fasting in humans.

Fasting upregulates adipose triglyceride lipase and hormone-sensitive lipase levels and phosphorylation in mouse kidney

2015 ◽  
Vol 93 (3) ◽  
pp. 262-267 ◽  
Author(s):  
Phillip M. Marvyn ◽  
Ryan M. Bradley ◽  
Emily B. Button ◽  
Emily B. Mardian ◽  
Robin E. Duncan
Keyword(s):  
Fatty Acids ◽  
Hormone Sensitive Lipase ◽  
Binding Motif ◽  
Adipose Triglyceride Lipase ◽  
Triglyceride Lipase ◽  
Protein Levels ◽  
Fasted State ◽  
Esterified Fatty Acids ◽  
Glomerular Filtrate ◽  
Hormone Sensitive

Circulating non-esterified fatty acids (NEFA) rise during fasting and are taken up by the kidneys, either directly from the plasma or during re-uptake of albumin from glomerular filtrate, and are stored as triacylglycerol (TAG). Subsequent utilization of stored fatty acids requires their hydrolytic release from cellular lipid droplets, but relatively little is known about renal lipolysis. We found that total [3H]triolein hydrolase activity of kidney lysates was significantly increased by 15% in the fasted state. Adipose triglyceride lipase (Atgl) and hormone-sensitive lipase (Hsl) mRNA expression was time-dependently increased by fasting, along with other fatty acid metabolism genes (Pparα, Cd36, and Aox). ATGL and HSL protein levels were also significantly induced (by 239 ± 7% and 322 ± 8%, respectively). Concomitant with changes in total protein levels, there was an increase in ATGL phosphorylation at the AMPK-regulated serine 406 site in the 14-3-3 binding motif, and an increase in HSL phosphorylation at serines 565 and 660 that are regulated by AMPK and PKA, respectively. Using immunofluorescence, we further demonstrate nearly ubiquitous expression of ATGL in the renal cortex with a concentration on the apical/lumenal surface of some cortical tubules. Our findings suggest a role for ATGL and HSL in kidney lipolysis.

scholarly journals Adipose triglyceride lipase expression in human adipose tissue and muscle. Role in insulin resistance and response to training and pioglitazone

Metabolism ◽  
2011 ◽  
Vol 60 (7) ◽  
pp. 1012-1020 ◽  
Author(s):  
Aiwei Yao-Borengasser ◽  
Vijayalakshmi Varma ◽  
Robert H. Coker ◽  
Gouri Ranganathan ◽  
Bounleut Phanavanh ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Adipose Triglyceride Lipase ◽  
Triglyceride Lipase ◽  
Lipase Expression

scholarly journals Adipose Triglyceride Lipase and Hormone-sensitive Lipase Are the Major Enzymes in Adipose Tissue Triacylglycerol Catabolism

2006 ◽  
Vol 281 (52) ◽  
pp. 40236-40241 ◽  
Author(s):  
Martina Schweiger ◽  
Renate Schreiber ◽  
Guenter Haemmerle ◽  
Achim Lass ◽  
Christian Fledelius ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Hormone Sensitive Lipase ◽  
Adipose Triglyceride Lipase ◽  
Triglyceride Lipase ◽  
Hormone Sensitive

LB-OR-5 THE ROLE OF ADIPOSE TRIGLYCERIDE LIPASE (ATGL) IN HUMAN ADIPOSE TISSUE LIPOLYSIS

2007 ◽  
Vol 8 (1) ◽  
pp. 228
Author(s):  
M. Schweiger ◽  
G. Schoiswohl ◽  
A. Lass ◽  
G. Haemmerle ◽  
R. Zechner ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Adipose Triglyceride Lipase ◽  
Triglyceride Lipase ◽  
Adipose Tissue Lipolysis

Effects of adipokine zinc-α2-glycoprotein on adipose tissue metabolism after dexamethasone treatment

2019 ◽  
Vol 44 (1) ◽  
pp. 83-89
Author(s):  
Yu Qiao ◽  
Guoqiang Fan ◽  
Jun Guo ◽  
Shixing Gao ◽  
Ruqian Zhao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Group Analysis ◽  
Adenosine Monophosphate ◽  
Experimental Models ◽  
Hormone Sensitive Lipase ◽  
Nonesterified Fatty Acid ◽  
Plasma Nefa ◽  
Lipid Mobilization ◽  
Protein Levels

Zinc-α2-glycoprotein (ZAG) has been demonstrated to play a role in stimulating lipid mobilization under normal conditions. However, further studies are required to determine whether ZAG overexpression can alleviate the reduction in plasma lipid levels under stress conditions. In the present study, we investigated the effects of ZAG on lipometabolism in white adipose tissue (WAT) after dexamethasone (DEX) stimulation using C57BL/6 male mice as the experimental models. Transcript and protein levels of genes associated with the β-adrenoreceptor (β-AR)/cyclic adenosine monophosphate/protein kinase a (PKA) pathway, lipid mobilization, and energy metabolism were determined by quantitative real-time polymerase chain reaction and Western blotting. Plasma levels of nonesterified fatty acid (NEFA) were measured using an automatic biochemical analyzer. Results indicated that plasma NEFA levels were decreased in the DEX group, but NEFA levels were rescued by ZAG overexpression. ZAG overexpression resulted in the upregulation of β3-AR and phosphorylated PKA protein relative to those of the DEX group. Analysis of lipometabolism showed that protein levels of phosphorylated hormone-sensitive lipase was reduced upon DEX treatment but were restored by ZAG overexpression. For energy metabolism, ZAG significantly upregulated the protein expression of carnitine palmitoyltransferase1a and cytochrome c oxidase subunit 1 relative to those of the DEX group. In conclusion, ZAG could alleviate DEX-induced decrease in plasma NEFA levels and this could be associated with the promoting lipid mobilization in WAT.

Novel regulatory roles of carboxylesterase 3 in lipid metabolism and browning in 3T3-L1 white adipocytes

2019 ◽  
Vol 44 (10) ◽  
pp. 1089-1098 ◽  
Author(s):  
Sulagna Mukherjee ◽  
Minji Choi ◽  
Jong Won Yun
Keyword(s):  
Lipid Metabolism ◽  
Cell Model ◽  
Hormone Sensitive Lipase ◽  
Marker Genes ◽  
Acid Oxidation ◽  
Adipose Triglyceride Lipase ◽  
Triglyceride Lipase ◽  
White Adipocytes ◽  
Enhanced Expression ◽  
Hormone Sensitive

The role of carboxylesterase 3 (Ces3) in the lipolysis of adipocytes has been overlooked, as 2 major lipolytic enzymes, hormone-sensitive lipase and adipose triglyceride lipase, play more powerful roles in lipolysis. In this study, we explored the effects of Ces3 in lipid metabolism by activating and inhibiting, as well as silencing, Ces3-encoding gene in 3T3-L1 cell model. Our results demonstrated that activation of Ces3 increased adipogenesis, and attenuated lipogenesis, whereas it promoted lipolysis and fatty acid oxidation. In addition, activated Ces3 led to enhanced expression of core fat browning marker genes and proteins, suggesting that Ces3 may play a pivotal role in fat browning and thermogenesis. In contrast, deficiency of Ces3 nullified the browning effect in white adipocytes, along with decreased adipogenesis in 3T3-L1 adipocytes. Interestingly, the expression pattern of adipose triglyceride lipase was in line with Ces3, whereas hormone-sensitive lipase was independently regulated irrespective of Ces3 expression levels, suggesting that Ces3 may play an important and compensatory role in the breakdown of triglycerides in white adipocytes. In conclusion, we provide the first evidence that activation of Ces3 contributes in the browning of white adipocytes, and maintains a balance in lipid metabolism, which could be a potential strategy in fighting against obesity.

scholarly journals PPARγ regulates adipose triglyceride lipase in adipocytes in vitro and in vivo

2007 ◽  
Vol 293 (6) ◽  
pp. E1736-E1745 ◽  
Author(s):  
Erin E. Kershaw ◽  
Michael Schupp ◽  
Hong-Ping Guan ◽  
Noah P. Gardner ◽  
Mitchell A. Lazar ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Protein Synthesis Inhibitor ◽  
Adipose Triglyceride Lipase ◽  
Dependent Manner ◽  
Triglyceride Lipase ◽  
Brown Adipose

Peroxisome proliferator-activated receptor-γ (PPARγ) regulates adipocyte genes involved in adipogenesis and lipid metabolism and is the molecular target for thiazolidinedione (TZD) antidiabetic agents. Adipose triglyceride lipase (ATGL) is a recently described triglyceride-specific lipase that is induced during adipogenesis and remains highly expressed in mature adipocytes. This study evaluates the ability of PPARγ to directly regulate ATGL expression in adipocytes in vitro and in vivo. In fully differentiated 3T3-L1 adipocytes, ATGL mRNA and protein are increased by TZD and non-TZD PPARγ agonists in a dose- and time-dependent manner. Rosiglitazone-mediated induction of ATGL mRNA is rapid and is not inhibited by the protein synthesis inhibitor cycloheximide, indicating that intervening protein synthesis is not required for this effect. Rosiglitazone-mediated induction of ATGL mRNA and protein is inhibited by the PPARγ-specific antagonist GW-9662 and is also significantly reduced following siRNA-mediated knockdown of PPARγ, supporting the direct transcriptional regulation of ATGL by PPARγ. In vivo, ATGL mRNA and protein are increased by rosiglitazone treatment in white and brown adipose tissue of mice with and without obesity due to high-fat diet or leptin deficiency. Thus, PPARγ positively regulates ATGL mRNA and protein expression in mature adipocytes in vitro and in adipose tissue in vivo, suggesting a role for ATGL in mediating PPARγ's effects on lipid metabolism.

Effects of DHEA on metabolic and endocrine functions of adipose tissue

2013 ◽  
Vol 14 (2) ◽  
Author(s):  
Joanna Karbowska ◽  
Zdzislaw Kochan
Keyword(s):  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Hormone Sensitive Lipase ◽  
Peroxisome Proliferator ◽  
Tissue Mass ◽  
Triacylglycerol Hydrolysis ◽  
Proliferation And Differentiation ◽  
Hormone Sensitive ◽  
Hormone Biosynthesis ◽  
Peroxisome Proliferator Activated Receptors

AbstractDehydroepiandrosterone (DHEA) and its sulfate ester, DHEAS, are the major circulating adrenal steroids and serve as substrates for sex hormone biosynthesis. DHEA is effectively taken up by adipose tissue, where the concentrations of free DHEA are four to ten times higher than those found in the circulation. DHEA reduces adipose tissue mass and inhibits the proliferation and differentiation of adipocytes; it may also protect against obesity by lowering the activity of stearoyl-CoA desaturase 1 in fat cells. Recent studies demonstrate that DHEA stimulates triacylglycerol hydrolysis in adipose tissue by increasing the expression and activity of adipose triglyceride lipase and hormone-sensitive lipase, the key enzymes of lipolysis. DHEA has been shown to modulate insulin signaling pathways, enhance glucose uptake in adipocytes, and increase insulin sensitivity in patients with DHEA deficiency or abnormal glucose tolerance. Additionally, by suppressing the activity of 11β-hydroxysteroid dehydrogenase 1 in adipocytes, DHEA may promote intra-adipose inactivation of cortisol to cortisone. Several studies have demonstrated that DHEA may also regulate the expression and secretion of adipokines such as leptin, adiponectin, and resistin. The effects of DHEA on adipokine expression in adipose tissue are depot-specific, with visceral fat being the most responsive. The mechanisms underlying DHEA actions in adipose tissue are still unclear; however, they involve nuclear receptors such as androgen receptor and peroxisome proliferator-activated receptors γ and α. Because clinical trials investigating the effects of DHEA failed to yield consistent results, further studies are needed to clarify the role of DHEA in the regulation of human adipose tissue physiology.

scholarly journals Comparative studies of the role of hormone-sensitive lipase and adipose triglyceride lipase in human fat cell lipolysis

2007 ◽  
Vol 292 (6) ◽  
pp. E1847-E1855 ◽  
Author(s):  
Mikael Rydén ◽  
Johan Jocken ◽  
Vanessa van Harmelen ◽  
Andrea Dicker ◽  
Johan Hoffstedt ◽  
...  
Keyword(s):  
Protein Expression ◽  
Polycystic Ovary ◽  
Human Mesenchymal Stem Cells ◽  
Hormone Sensitive Lipase ◽  
Adipose Triglyceride Lipase ◽  
Human Adipocytes ◽  
Fat Cell ◽  
Triglyceride Lipase ◽  
Knock Down ◽  
Hormone Sensitive

Hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) regulate adipocyte lipolysis in rodents. The purpose of this study was to compare the roles of these lipases for lipolysis in human adipocytes. Subcutaneous adipose tissue was investigated. HSL and ATGL protein expression were related to lipolysis in isolated mature fat cells. ATGL or HSL were knocked down by RNA interference (RNAi) or selectively inhibited, and effects on lipolysis were studied in differentiated preadipocytes or adipocytes derived from human mesenchymal stem cells (hMSC). Subjects were all women. There were 12 lean controls, 8 lean with polycystic ovary syndrome (PCOS), and 27 otherwise healthy obese subjects. We found that norepinephrine-induced lipolysis was positively correlated with HSL protein levels ( P < 0.0001) but not with ATGL protein. Women with PCOS or obesity had significantly decreased norepinephrine-induced lipolysis and HSL protein expression but no change in ATGL protein expression. HSL knock down by RNAi reduced basal and catecholamine-induced lipolysis. Knock down of ATGL decreased basal lipolysis but did not change catecholamine-stimulated lipolysis. Treatment of hMSC with a selective HSL inhibitor during and/or after differentiation in adipocytes reduced basal lipolysis by 50%, but stimulated lipolysis was inhibited completely. In contrast to findings in rodents, ATGL is of less importance than HSL in regulating catecholamine-induced lipolysis and cannot replace HSL when this enzyme is continuously inhibited. However, both lipases regulate basal lipolysis in human adipocytes. ATGL expression, unlike HSL, is not influenced by obesity or PCOS.

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