scholarly journals Exercise Training Effects on Inflammatory Gene Expression in White Adipose Tissue of Young Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Tracy Baynard ◽  
Victoria J. Vieira-Potter ◽  
Rudy J. Valentine ◽  
Jeffrey A. Woods
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Exercise Training ◽  
White Adipose Tissue ◽  
Training Effects ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Young Mice

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.

Pro-inflammatory gene expression in adipose tissue in patients with atherosclerosis

2016 ◽  
Vol 252 ◽  
pp. e174 ◽  
Author(s):  
S. Čejková ◽  
I. Králová Lesná ◽  
J. Froněk ◽  
A. Králová ◽  
R. Poledne
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

Inflammation, but not recruitment, of adipose tissue macrophages requires signalling through Mac-1 (CD11b/CD18) in diet-induced obesity (DIO)

2017 ◽  
Vol 117 (02) ◽  
pp. 325-338 ◽  
Author(s):  
Dennis Wolf ◽  
Nora Bukosza ◽  
David Engel ◽  
Marjorie Poggi ◽  
Felix Jehle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Inflammatory Gene Expression ◽  
Tissue Inflammation ◽  
Inflammatory Gene ◽  
Diet Induced Obesity ◽  
Adipose Tissue Macrophages ◽  
Cell Accumulation

SummaryCell accumulation is a prerequisite for adipose tissue inflammation. The leukocyte integrin Mac-1 (CD11b/CD18, αMβ2) is a classic adhesion receptor critically regulating inflammatory cell recruitment. Here, we tested the hypothesis that a genetic deficiency and a therapeutic modulation of Mac-1 regulate adipose tissue inflammation in a mouse model of diet-induced obesity (DIO). C57Bl6/J mice genetically deficient (Mac-1-/-) or competent for Mac-1 (WT) consumed a high fat diet for 20 weeks. Surprisingly, Mac-1-/- mice presented with increased diet-induced weight gain, decreased insulin sensitivity in skeletal muscle and in the liver in insulin-clamps, insulin secretion deficiency and elevated glucose levels in fasting animals, and dyslipidaemia. Unexpectedly, accumulation of adipose tissue macrophages (ATMs) was unaffected, while gene expression indicated less inflamed adipose tissue and macrophages in Mac-1-/- mice. In contrast, inflammatory gene expression at distant locations, such as in skeletal muscle, was not changed. Treatment of ATMs with an agonistic anti-Mac-1 antibody, M1/70, induced pro-inflammatory genes in cell culture. In vivo, treatment with M1/70 induced a hyper-inflammatory phenotype with increased expression of IL-6 and MCP-1, whereas accumulation of ATMs did not change. Finally, inhibition of Mac-1’s adhesive interaction to CD40L by the peptide inhibitor cM7 did not affect myeloid cell accumulation in adipose tissue. We present the surprising finding that adhesive properties of the leukocyte integrin Mac-1 are not required for macrophage accumulation in adipose tissue. Instead, Mac-1 modulates inflammatory gene expression in macrophages. These findings question the net effect of integrin blockade in cardio-metabolic disease.D. W., N. B., and D. E. equally contributed to this work.K. P., E. L., and A. Z. share senior authorship.Note: The review process for this manuscript was fully handled by Gregory Y. H. Lip, Editor in Chief.Supplementary Material to this article is available online at www.thrombosis-online.com.

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