Inflammatory Response in White Adipose Tissue in the Non-Obese Hormone-Sensitive Lipase Null Mouse Model

2006 ◽  
Vol 5 (7) ◽  
pp. 1701-1710 ◽  
Author(s):  
Ola Hansson ◽  
Kristoffer Ström ◽  
Nuray Güner ◽  
Nils Wierup ◽  
Frank Sundler ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Response ◽  
Mouse Model ◽  
White Adipose Tissue ◽  
Hormone Sensitive Lipase ◽  
Null Mouse ◽  
Hormone Sensitive

Seasonal changes in hormone-sensitive and lipoprotein lipase mRNA concentrations in marmot white adipose tissue

1992 ◽  
Vol 262 (2) ◽  
pp. R177-R181 ◽  
Author(s):  
B. E. Wilson ◽  
S. Deeb ◽  
G. L. Florant
Keyword(s):  
Adipose Tissue ◽  
Lipoprotein Lipase ◽  
White Adipose Tissue ◽  
Mass Gain ◽  
The Body ◽  
Hormone Sensitive Lipase ◽  
Marmota Flaviventris ◽  
Fasting Period ◽  
Hormone Sensitive ◽  
Clear Increase

White adipose tissue (WAT) and plasma samples were obtained from yellow-bellied marmots (Marmota flaviventris) throughout the year. Mean plasma triacylglycerol (TG), free fatty acids (FFAs), and glycerol were determined. There was a clear increase in FFAs and decrease in mean TG and glycerol during the hibernation period when animals were fasting, suggesting increased lipolysis. RNA was isolated from WAT biopsies at four times in the year: spring, summer, fall, and winter. There were significant changes in the relative levels of mRNA for lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) during the body mass cycle of the marmot. The relative levels of LPL mRNA are high during the mass gain phase of the year and that of HSL mRNA are high during the fasting period when endogenous lipid is utilized. These results suggest that the genes for LPL and HSL are regulated seasonally to control the adipose mass depot in marmots.

scholarly journals Acetylation of Cavin-1 Promotes Lipolysis in White Adipose Tissue

2017 ◽  
Vol 37 (16) ◽  
Author(s):  
Shui-Rong Zhou ◽  
Liang Guo ◽  
Xu Wang ◽  
Yang Liu ◽  
Wan-Qiu Peng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Molecular Mechanisms ◽  
Hormone Sensitive Lipase ◽  
Dependent Manner ◽  
Nutritional Regulation ◽  
Fat Mobilization ◽  
Hormone Sensitive ◽  
Shed Light

ABSTRACT White adipose tissue (WAT) serves as a reversible energy storage depot in the form of lipids in response to nutritional status. Cavin-1, an essential component in the biogenesis of caveolae, is a positive regulator of lipolysis in adipocytes. However, molecular mechanisms of cavin-1 in the modulation of lipolysis remain poorly understood. Here, we showed that cavin-1 was acetylated at lysines 291, 293, and 298 (3K), which were under nutritional regulation in WAT. We further identified GCN5 as the acetyltransferase and Sirt1 as the deacetylase of cavin-1. Acetylation-mimetic 3Q mutants of cavin-1 augmented fat mobilization in 3T3-L1 adipocytes and zebrafish. Mechanistically, acetylated cavin-1 preferentially interacted with hormone-sensitive lipase and recruited it to the caveolae, thereby promoting lipolysis. Our findings shed light on the essential role of cavin-1 in regulating lipolysis in an acetylation-dependent manner in WAT.

Hormone-sensitive lipase-independent adipocyte lipolysis during β-adrenergic stimulation, fasting, and dietary fat loading

2004 ◽  
Vol 287 (2) ◽  
pp. E282-E288 ◽  
Author(s):  
Mélanie Fortier ◽  
Shu Pei Wang ◽  
Pascale Mauriège ◽  
Meriem Semache ◽  
Léandra Mfuma ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
White Adipose Tissue ◽  
Dietary Fat ◽  
Intraperitoneal Administration ◽  
Hormone Sensitive Lipase ◽  
Adrenergic Stimulation ◽  
Hormone Sensitive ◽  
Isolated Adipocytes

In white adipose tissue, lipolysis can occur by hormone-sensitive lipase (HSL)-dependent or HSL-independent pathways. To study HSL-independent lipolysis, we placed HSL-deficient mice in conditions of increased fatty acid flux: β-adrenergic stimulation, fasting, and dietary fat loading. Intraperitoneal administration of the β3-adrenergic agonist CL-316243 caused a greater increase in nonesterified fatty acid level in controls (0.33 ± 0.05 mmol/l) than in HSL−/− mice (0.12 ± 0.01 mmol/l, P < 0.01). Similarly, in isolated adipocytes, lipolytic response to CL-316243 was greatly reduced in HSL−/− mice compared with controls. Fasting for ≤48 h produced normal mobilization and oxidation of fatty acids in HSL−/− mice, as judged by similar values of respiratory quotient and oxygen consumption as in HSL+/+ controls. In isolated adipocytes, lipolysis in the absence of β-adrenergic stimulation was 1.9-fold greater in HSL−/− than in HSL+/+ cells ( P < 0.05), increasing to 6.5-fold after fasting ( P < 0.01). After 6 wk of a fat-rich diet containing 31.5% of energy as lipid, weight gain of HSL−/− mice was 4.4-fold less than in HSL+/+ mice ( P < 0.01), and total abdominal fat mass was 5.2-fold lower in HSL−/− than in HSL+/+ mice ( P < 0.01). In white adipose tissue, HSL is essential for normal acute β-adrenergic-stimulated lipolysis and permits normal triglyceride storage capacity in response to dietary fat loading. However, HSL-independent lipolysis can markedly increase during fasting, both in isolated adipocytes and in intact mice, and can mediate a normal flux of fatty acids during fasting.

Role of hormone-sensitive lipase in β-adrenergic remodeling of white adipose tissue

2007 ◽  
Vol 293 (5) ◽  
pp. E1188-E1197 ◽  
Author(s):  
Emilio P. Mottillo ◽  
Xiang Jun Shen ◽  
James G. Granneman
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Mitochondrial Biogenesis ◽  
Oxidative Capacity ◽  
Hormone Sensitive Lipase ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Hormone Sensitive

Free fatty acids (FFA) are important extracellular and intracellular signaling molecules and are thought to be involved in β-adrenergic-induced remodeling of adipose tissue, which involves a transient inflammatory response followed by mitochondrial biogenesis and increased oxidative capacity. This work examined the role of hormone-sensitive lipase (HSL), a key enzyme of acylglycerol metabolism, in white adipose tissue (WAT) remodeling using genetic inactivation or pharmacological inhibition. Acute treatment with the β3-adrenergic agonist CL-316,243 (CL) induced expression of inflammatory markers and caused extravasation of myeloid cells in WAT of wild-type (WT) mice. HSL-knockout (KO) mice had elevated inflammatory gene expression in the absence of stimulation, and acute injection of CL did not further recruit myeloid cells, nor did it further elevate inflammatory gene expression. Acute pharmacological inhibition of HSL with BAY 59-9435 (BAY) had no effect on inflammatory gene expression in WAT or in cultured 3T3-L1 adipocytes. However, BAY prevented induction of inflammatory cytokines by β-adrenergic stimulation in WAT in vivo and in cultured 3T3-L1 adipocytes. Chronic CL treatment stimulated mitochondrial biogenesis, expanded oxidative capacity, and increased lipid droplet fragmentation in WT mice, and these effects were significantly impaired in HSL-KO mice. In contrast to HSL-KO mice, mice with defective signaling of Toll-like receptor 4, a putative FFA receptor, showed normal β-adrenergic-induced remodeling of adipose tissue. Overall, results reveal the importance of HSL activity in WAT metabolic plasticity and inflammation.

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