Biochemical activities of tubercidin 3', 5'-cyclic monophosphate in rat epididymal adipose tissue

1971 ◽  
Vol 20 (1) ◽  
pp. 249-251 ◽  
Author(s):  
Melvin Blecher ◽  
J.T. Ro'ane ◽  
P.D. Flynn
Keyword(s):  
Adipose Tissue ◽  
Epididymal Adipose Tissue ◽  
Cyclic Monophosphate

scholarly journals Olive Leaf Extract Attenuates Obesity in High-Fat Diet-Fed Mice by Modulating the Expression of Molecules Involved in Adipogenesis and Thermogenesis

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Ying Shen ◽  
Su Jin Song ◽  
Narae Keum ◽  
Taesun Park
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Leaf Extract ◽  
Body Weight Gain ◽  
Plasma Lipid ◽  
Epididymal Adipose Tissue ◽  
Chow Diet ◽  
Olive Leaf ◽  
High Fat ◽  
Olive Leaf Extract

The present study aimed to investigate whether olive leaf extract (OLE) prevents high-fat diet (HFD)-induced obesity in mice and to explore the underlying mechanisms. Mice were randomly divided into groups that received a chow diet (CD), HFD, or 0.15% OLE-supplemented diet (OLD) for 8 weeks. OLD-fed mice showed significantly reduced body weight gain, visceral fat-pad weights, and plasma lipid levels as compared with HFD-fed mice. OLE significantly reversed the HFD-induced upregulation of WNT10b- and galanin-mediated signaling molecules and key adipogenic genes (PPARγ, C/EBPα, CD36, FAS, and leptin) in the epididymal adipose tissue of HFD-fed mice. Furthermore, the HFD-induced downregulation of thermogenic genes involved in uncoupled respiration (SIRT1, PGC1α, and UCP1) and mitochondrial biogenesis (TFAM, NRF-1, and COX2) was also significantly reversed by OLE. These results suggest that OLE exerts beneficial effects against obesity by regulating the expression of genes involved in adipogenesis and thermogenesis in the visceral adipose tissue of HFD-fed mice.

Effect of Hypophysectomy on the Metabolism of Epididymal Adipose Tissue

Endocrinology ◽  
1964 ◽  
Vol 75 (2) ◽  
pp. 222-225 ◽  
Author(s):  
RICHARD SANDLER ◽  
M. GUILLERMO HERRERA ◽  
ALBERT E. RENOLD
Keyword(s):  
Adipose Tissue ◽  
Epididymal Adipose Tissue

scholarly journals Triglyceride Synthesis in Epididymal Adipose Tissue

2008 ◽  
Vol 284 (10) ◽  
pp. 6101-6108 ◽  
Author(s):  
Ilya R. Bederman ◽  
Steven Foy ◽  
Visvanathan Chandramouli ◽  
James C. Alexander ◽  
Stephen F. Previs
Keyword(s):  
Adipose Tissue ◽  
Epididymal Adipose Tissue ◽  
Triglyceride Synthesis

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.

Metabolic influences on enzymes of glycogen synthesis and breakdown in adipose tissue

1964 ◽  
Vol 207 (6) ◽  
pp. 1215-1220 ◽  
Author(s):  
Alisa Gutman ◽  
Eleazar Shafrir
Keyword(s):  
Adipose Tissue ◽  
Protein Content ◽  
Glycogen Synthesis ◽  
Total Activity ◽  
Epididymal Adipose Tissue ◽  
Control Value ◽  
Prolonged Fast ◽  
Rat Adipose Tissue

Rat adipose tissue from different body sites was shown to contain uridine diphosphoglucose (UDPG)-transglucosylase activity, which on the basis of protein content was comparable to or higher than that reported for muscle or liver. In epididymal adipose tissue, the activity of UDPG-glycogen transglucosylase and phosphorylase, as well as the content of glycogen per wet weight, decreased with increasing age of the animals in parallel with the decrease of tissue protein content. On prolonged fast the activity of UDPG-glycogen transglucosylase and phosphorylase per milligram protein dropped by 25–50% of the control value. On refeeding, the extent of changes was variable but, in general, at 24 hr control or higher levels of activity were reached and at 48 hr the activities were elevated. The ratio of glucose 6-phosphate independent activity of UDPG-glycogen transglucosylase to total activity was not affected by fasting and refeeding or by the administration of glucose with insulin. In adrenalectomized rats, with high adipose tissue glycogen, no change in UDPG-glycogen transglucosylase was found, whereas the levels of phosphorylase were elevated. Epinephrine in vivo and in vitro did not affect the activity of UDPG-glycogen transglucosylase of adipose tissue.

scholarly journals Indoxyl Sulfate Contributes to Adipose Tissue Inflammation through the Activation of NADPH Oxidase

Toxins ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 502
Author(s):  
Shoma Tanaka ◽  
Hiroshi Watanabe ◽  
Takehiro Nakano ◽  
Tadashi Imafuku ◽  
Hiromasa Kato ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Nadph Oxidase ◽  
Organic Anion ◽  
Indoxyl Sulfate ◽  
Epididymal Adipose Tissue ◽  
Ros Production ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Anion Transporter

Adipose tissue inflammation appears to be a risk factor for the progression of chronic kidney disease (CKD), but the effect of CKD on adipose tissue inflammation is poorly understood. The purpose of this study was to clarify the involvement of uremic toxins (indoxyl sulfate (IS), 3-indoleacetic acid, p-cresyl sulfate and kynurenic acid) on CKD-induced adipose tissue inflammation. IS induces monocyte chemoattractant protein-1 (MCP-1) expression and reactive oxygen species (ROS) production in the differentiated 3T3L-1 adipocyte. An organic anion transporter (OAT) inhibitor, an NADPH oxidase inhibitor or an antioxidant suppresses the IS-induced MCP-1 expression and ROS production, suggesting the OAT/NADPH oxidase/ROS pathway is involved in the action of IS. Co-culturing 3T3L-1 adipocytes and mouse macrophage cells showed incubating adipocytes with IS increased macrophage infiltration. An IS-overload in healthy mice increased IS levels, oxidative stress and MCP-1 expression in epididymal adipose tissue compared to unloaded mice. Using 5/6-nephrectomized mice, the administration of AST-120 suppressed oxidative stress and the expression of MCP-1, F4/80 and TNF-α in epididymal adipose tissue. These collective data suggest IS could be a therapeutic target for the CKD-related inflammatory response in adipose tissue, and that AST-120 could be useful for the treatment of IS-induced adipose tissue inflammation.

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