scholarly journals Adipose Tissue Hypoxia, Inflammation, and Fibrosis in Obese Insulin-Sensitive and Obese Insulin-Resistant Subjects

2016 ◽  
Vol 101 (4) ◽  
pp. 1422-1428 ◽  
Author(s):  
Helen M. Lawler ◽  
Chantal M. Underkofler ◽  
Philip A. Kern ◽  
Christopher Erickson ◽  
Brooke Bredbeck ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Tissue Hypoxia ◽  
Insulin Resistant

Does intra-abdominal adipose tissue in black men determine whether NIDDM is insulin-resistant or insulin-sensitive?

Diabetes ◽  
1995 ◽  
Vol 44 (2) ◽  
pp. 141-146 ◽  
Author(s):  
M. A. Banerji ◽  
R. L. Chaiken ◽  
D. Gordon ◽  
J. G. Kral ◽  
H. E. Lebovitz
Keyword(s):  
Adipose Tissue ◽  
Black Men ◽  
Abdominal Adipose Tissue ◽  
Insulin Resistant

JNK and IKKβ phosphorylation is reduced by glucocorticoids in adipose tissue from insulin-resistant rats

2015 ◽  
Vol 145 ◽  
pp. 1-12 ◽  
Author(s):  
Katia Motta ◽  
Amanda Marreiro Barbosa ◽  
Franciane Bobinski ◽  
Antonio Carlos Boschero ◽  
Alex Rafacho
Keyword(s):  
Adipose Tissue ◽  
Insulin Resistant

scholarly journals Exercise training enhances white adipose tissue metabolism in rats selectively bred for low- or high-endurance running capacity

2013 ◽  
Vol 305 (3) ◽  
pp. E429-E438 ◽  
Author(s):  
Erin J. Stephenson ◽  
Sarah J. Lessard ◽  
Donato A. Rivas ◽  
Matthew J. Watt ◽  
Ben B. Yaspelkis ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
White Adipose Tissue ◽  
Citrate Synthase ◽  
Mitochondrial Protein ◽  
Treadmill Running ◽  
Endurance Running ◽  
Insulin Resistant ◽  
Disease States ◽  
Hcr Model

Impaired visceral white adipose tissue (WAT) metabolism has been implicated in the pathogenesis of several lifestyle-related disease states, with diminished expression of several WAT mitochondrial genes reported in both insulin-resistant humans and rodents. We have used rat models selectively bred for low- (LCR) or high-intrinsic running capacity (HCR) that present simultaneously with divergent metabolic phenotypes to test the hypothesis that oxidative enzyme expression is reduced in epididymal WAT from LCR animals. Based on this assumption, we further hypothesized that short-term exercise training (6 wk of treadmill running) would ameliorate this deficit. Approximately 22-wk-old rats (generation 22) were studied. In untrained rats, the abundance of mitochondrial respiratory complexes I–V, citrate synthase (CS), and PGC-1 was similar for both phenotypes, although CS activity was greater than 50% in HCR ( P = 0.09). Exercise training increased CS activity in both phenotypes but did not alter mitochondrial protein content. Training increased the expression and phosphorylation of proteins with roles in β-adrenergic signaling, including β3-adrenergic receptor (16% increase in LCR; P < 0.05), NOR1 (24% decrease in LCR, 21% decrease in HCR; P < 0.05), phospho-ATGL (25% increase in HCR; P < 0.05), perilipin (25% increase in HCR; P < 0.05), CGI-58 (15% increase in LCR; P < 0.05), and GLUT4 (16% increase in HCR; P < 0.0001). A training effect was also observed for phospho-p38 MAPK (12% decrease in LCR, 20% decrease in HCR; P < 0.05) and phospho-JNK (29% increase in LCR, 20% increase in HCR; P < 0.05). We conclude that in the LCR-HCR model system, mitochondrial protein expression in WAT is not affected by intrinsic running capacity or exercise training. However, training does induce alterations in the activity and expression of several proteins that are essential to the intracellular regulation of WAT metabolism.

Adipose tissue hypoxia and insulin resistance

2016 ◽  
Vol 64 (4) ◽  
pp. 830-832 ◽  
Author(s):  
Neda Rasouli
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Hypoxia ◽  
Sequence Of Events ◽  
Adipose Tissue Dysfunction ◽  
Underlying Mechanisms ◽  
Key Events

Despite the well-established association of obesity with insulin resistance and inflammation, the underlying mechanisms and sequence of events leading to inflammation and insulin resistance remain unknown. Adipose tissue hypoxia has been proposed as one of the possible key events during the process of fat expansion that leads to adipose tissue dysfunction. The focus of this paper is reviewing the evidence on adipose tissue hypoxia in obesity and its relation to insulin resistance.

Cell Non-Autonomous Regulation of Aging and Mitochondrial Uncoupling by Insulin-Resistant Adipose Tissue

2011 ◽  
pp. P3-388-P3-388
Author(s):  
Steven J Russell ◽  
Carly Cederquist ◽  
Ji Sun Park ◽  
Marcelo A Mori ◽  
C Ronald Kahn
Keyword(s):  
Adipose Tissue ◽  
Mitochondrial Uncoupling ◽  
Insulin Resistant ◽  
Autonomous Regulation

scholarly journals High-salt intake induced visceral adipose tissue hypoxia and its association with circulating monocyte subsets in humans

Obesity ◽  
2014 ◽  
Vol 22 (6) ◽  
pp. 1470-1476 ◽  
Author(s):  
Xin Zhou ◽  
Fei Yuan ◽  
Wen-Jie Ji ◽  
Zhao-Zeng Guo ◽  
Ling Zhang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Salt Intake ◽  
Tissue Hypoxia ◽  
High Salt ◽  
Monocyte Subsets ◽  
High Salt Intake ◽  
Visceral Adipose

scholarly journals Specific Preservation of Biosynthetic Responses to Insulin in Adipose Tissue May Contribute to Hyperleptinemia in Insulin-Resistant Obese Mice

2004 ◽  
Vol 134 (5) ◽  
pp. 1045-1050 ◽  
Author(s):  
Tooru M. Mizuno ◽  
Toshiya Funabashi ◽  
Steven P. Kleopoulos ◽  
Charles V. Mobbs
Keyword(s):  
Adipose Tissue ◽  
Obese Mice ◽  
Insulin Resistant

Alterations of the classic pathway of complement in adipose tissue of obesity and insulin resistance

2007 ◽  
Vol 292 (5) ◽  
pp. E1433-E1440 ◽  
Author(s):  
Jinhui Zhang ◽  
Wendy Wright ◽  
David A. Bernlohr ◽  
Samuel W. Cushman ◽  
Xiaoli Chen
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Epididymal Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Insulin Resistant ◽  
Obese Rats ◽  
Initial Activation ◽  
Adipose Cells ◽  
Classic Pathway

Adipose tissue inflammation has recently been linked to the pathogenesis of obesity and insulin resistance. C1 complex comprising three distinct proteins, C1q, C1r, and C1s, involves the key initial activation of the classic pathway of complement and plays an important role in the initiation of inflammatory process. In this study, we investigated adipose expression and regulation of C1 complement subcomponents and C1 activation regulator decorin in obesity and insulin resistance. Expression of C1q in epididymal adipose tissue was increased consistently in ob/ob mice, Zucker obese rats, and high fat-diet-induced obese (HF-DIO) mice. Decorin was found to increase in expression in Zucker obese rats and HF-DIO mice but decrease in ob/ob mice. After TZD administration, C1q and decorin expression was reversed in Zucker obese rats and HF-DIO mice. Increased expression of C1 complement and decorin was observed in both primary adipose and stromal vascular cells isolated from Zucker obese rats. Upregulation of C1r and C1s expression was also perceived in adipose cells from insulin-resistant humans. Furthermore, expression of C1 complement and decorin is dysregulated in TNF-α-induced insulin resistance in 3T3-L1 adipocytes and cultured rat adipose cells as they become insulin resistant after 24-h culture. These data suggests that both adipose and immune cells are the sources for abnormal adipose tissue production of C1 complement and decorin in obesity. Our findings also demonstrate that excessive activation of the classic pathway of complement commonly occurs in obesity, suggesting its possible role in adipose tissue inflammation and insulin resistance.

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