Acute Up-Regulation of Adipose Triglyceride Lipase and Release of Non-Esterified Fatty Acids by Dexamethasone in Chicken Adipose Tissue

Lipids ◽  
2011 ◽  
Vol 46 (9) ◽  
pp. 813-820 ◽  
Author(s):  
Julie Serr ◽  
Yeunsu Suh ◽  
Shin-Ae Oh ◽  
Sangsu Shin ◽  
Minseok Kim ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Adipose Triglyceride Lipase ◽  
Triglyceride Lipase ◽  
Esterified Fatty Acids

scholarly journals Adipose triglyceride lipase in immune response, inflammation, and atherosclerosis

2012 ◽  
Vol 393 (9) ◽  
pp. 1005-1011 ◽  
Author(s):  
Branislav Radovic ◽  
Elma Aflaki ◽  
Dagmar Kratky
Keyword(s):  
Fatty Acids ◽  
Energy Homeostasis ◽  
Current Knowledge ◽  
Cell Types ◽  
Adipose Triglyceride Lipase ◽  
Hydrolytic Cleavage ◽  
Central Importance ◽  
Energy Substrate ◽  
Triglyceride Lipase ◽  
Esterified Fatty Acids

Abstract Consistent with its central importance in lipid and energy homeostasis, lipolysis occurs in essentially all tissues and cell types, including macrophages. The hydrolytic cleavage of triacylglycerol by adipose triglyceride lipase (ATGL) generates non-esterified fatty acids, which are subsequently used as essential precursors for lipid and membrane synthesis, mediators in cell signaling processes or as energy substrate in mitochondria. This review summarizes the current knowledge concerning the consequences of ATGL deficiency in macrophages with particular emphasis on macrophage (dys)-function, apoptosis, and atherosclerosis.

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.

Effect of Propolis-Supplemented Diet on Body Composition and Endocrine Function of Adipose Tissue

2020 ◽  
Vol 19 (2) ◽  
pp. 217-221
Author(s):  
Maria Jesús Lisbona-González ◽  
Candela Reyes-Botella ◽  
Esther Muñoz-Soto ◽  
Maria Victoria Olmedo-Gaya, ◽  
Jorge Moreno-Fernandez ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Composition ◽  
Adipose Tissue ◽  
Endocrine Function ◽  
Control Group ◽  
Albino Rats ◽  
Standard Diet ◽  
Reduced Body ◽  
Esterified Fatty Acids ◽  
Wistar Albino Rats

Adipose tissue is an endocrine organ and has central role in interaction with other organs or tissues while propolis can induce lipolysis. Therefore, the aim of this study is to provide detailed information about adipose tissue homeostasis modifications and body composition during propolis supplement consumption. Twenty male Wistar albino rats (8 weeks) were divided into two groups of 10 animals each and fed for 90 days with two different types of diets: standard for the control group (diet C) and standard diet + 2% propolis (diet P). Thyroid hormones did not show differences, while ghrelin and adiponectin decreased in the group that was fed propolis. Insulin, leptin, and non-esterified fatty acids also increased along with reduced body weight and fat, in addition to increased lean mass when propolis was in the diet. We conclude that propolis could decrease ghrelin and adiponectin but increase non-esterified fatty acids and insulin secretion, which improves body composition.

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.

scholarly journals Release of Non-Esterified Fatty Acids from Adipose Tissue in Normal and Diabetic Rats

Nature ◽  
1959 ◽  
Vol 184 (4693) ◽  
pp. 1147-1147 ◽  
Author(s):  
J. WENKEOVÁ ◽  
J. PÁV
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Diabetic Rats ◽  
Esterified Fatty Acids

scholarly journals Hypoxia-inducible lipid droplet-associated interacts with DGAT1 and promotes lipid storage in hepatocytes

2020 ◽  
Author(s):  
Montserrat A. de la Rosa Rodriguez ◽  
Anne Gemmink ◽  
Michel van Weeghel ◽  
Marie Louise Aoun ◽  
Christina Warnecke ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Lipid Droplet ◽  
Hepatoma Cell ◽  
Lipid Storage ◽  
Adipose Triglyceride Lipase ◽  
Dgat Activity ◽  
Triglyceride Synthesis ◽  
Alcoholic Fatty Liver ◽  
Triglyceride Lipase ◽  
Associated Proteins

ABSTRACTLipid droplets (LD) are dynamic organelles that can expand and shrink, driven by fluctuations in the rate of triglyceride synthesis and degradation. Triglyceride synthesis, storage in LD, and degradation are governed by a complex set of LD-associated proteins. One of these LD-associated proteins, hypoxia-inducible lipid droplet-associated (HILPDA), was found to impair LD breakdown by inhibiting adipose triglyceride lipase. Here we characterized the physiological role and mechanism of action of HILPDA in hepatocytes. Expression of HILPDA was induced by fatty acids in several hepatoma cell lines. Hepatocyte-specific deficiency of HILPDA in mice modestly but significantly reduced hepatic triglycerides in mice with non-alcoholic fatty liver disease. Similarly, deficiency of HILPDA in mouse precision-cut liver slices and primary hepatocytes reduced lipid storage and accumulation of fluorescently-labelled fatty acids in LD, respectively, which was independent of adipose triglyceride lipase. Fluorescence microscopy showed that HILPDA partly colocalizes with LD and with the endoplasmic reticulum, is especially abundant in perinuclear areas, and mainly associates with newly added fatty acids. Real-time fluorescence live-cell imaging further revealed that HILPDA preferentially localizes to LD that are being remodelled. Mechanistically, HILPDA overexpression increased lipid storage in human hepatoma cells concomitant with an increase in DGAT activity and DGAT1 protein levels. Finally, confocal microscopy and Förster resonance energy transfer-fluorescence lifetime imaging microscopy analysis indicated that HILPDA colocalizes and physically interacts with DGAT1. Overall, our data indicate that HILPDA physically interacts with DGAT1 and increases DGAT activity. These findings suggest a novel mechanism in hepatocytes that links elevated fatty acid levels to stimulation of triglyceride synthesis and storage.

THE EFFECT OF VARIOUS SACCHARIDES ON THE RELEASE OF NON ESTERIFIED FATTY ACIDS FROM ADIPOSE TISSUE IN VITRO

1962 ◽  
Vol 40 (4) ◽  
pp. 455-458 ◽  
Author(s):  
W. F. Perry ◽  
R. J. Tjaden
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Incubation Medium ◽  
Epididymal Adipose Tissue ◽  
Tissue Cell ◽  
Glycerol Phosphate ◽  
Esterified Fatty Acids ◽  
Adipose Tissue Cell ◽  
Other Substances

Rat epididymal adipose tissue was incubated in a phosphate–albumin medium to ascertain the effect of various saccharides and other substances on the release of non-esterified fatty acids (NEFA) into the medium. It was found that incubation with glucose, mannose, fructose, and 2-deoxy glucose resulted in less release of NEFA from the tissue into the incubation medium. Incubation with galactose, sucrose, lactose, D-ribose, D-xylose, L-xylose, D-arabinose, L-arabinose, D-lyxose, sodium pyruvate, glycerol, and glycerol phosphate showed no differences from the control in release of NEFA into the incubation medium. These results are consistent with the theory that the NEFA-lowering action of glucose is due to esterification of free fatty acid within the adipose tissue cell by glycerol phosphate.

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