High-fat diet–induced obesity and insulin resistance were ameliorated via enhanced fecal bile acid excretion in tumor necrosis factor-alpha receptor knockout mice

2011 ◽  
Vol 359 (1-2) ◽  
pp. 161-167 ◽  
Author(s):  
Mayumi Yamato ◽  
Takeshi Shiba ◽  
Tomomi Ide ◽  
Naoko Seri ◽  
Wataru Kudo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Tumor Necrosis ◽  
Fecal Bile Acid ◽  
Acid Excretion ◽  
High Fat ◽  
Necrosis Factor Alpha ◽  
Diet Induced Obesity ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor Alpha Knockout Promotes Adipose Fatty Acid Oxidation and Attenuates Insulin Resistance and Hepatic Steatosis in High Fat Diet-Fed Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1705-1705
Author(s):  
Seok-Yeong Yu ◽  
Jinchao Li ◽  
Zhenhua Liu ◽  
Young-Cheul Kim
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
High Fat Diet ◽  
Tumor Necrosis ◽  
Acid Metabolism ◽  
Acid Oxidation ◽  
High Fat ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Abstract Objectives Substantial evidence indicates that adipose tissue (AT) dysfunction and lipid spillover in obesity promote insulin resistance and non-alcoholic fatty liver disease. Tumor necrosis factor alpha (TNFα) is one of the pro-inflammatory cytokines overexpressed in obesity and its knockout (KO) attenuates diet-induced adiposity, lipid deposition in the liver and insulin resistance. However, the potential roles played by TNFα in fatty acid metabolism in AT have been incompletely understood. The objective of this study was to investigate the role of TNFα in obesity-induced insulin resistance with the goal of providing a potential target for therapeutics. Methods Three groups of wild type (WT) or TNFα KO male mice on the same B6 genetic background were fed designated diets for 16 weeks; WT fed a low-fat diet (LFD-WT), WT fed a high-fat diet (HFD-WT), and TNFα KO fed a HFD (HFD-TNFα KO). Blood concentrations of glucose and insulin and hepatic triacylglycerol (TG) levels were measured. The expression of genes involved in fatty acid and TG synthesis and fatty acid oxidation (FAO) was measured in epididymal white AT (eWAT). Results Compared to the LFD-fed mice, HFD-WT group had a significantly higher levels of blood glucose and insulin, and hepatic TG (P < 0.05). TNFα KO mice significantly improved HFD-induced hyperglycemia, hyperinsulinemia and hepatic TG accumulation (P < 0.05). In eWAT, TNFα ablation did not affect the expression of de novo fatty-acid synthesis-related genes, but significantly increased the expression of TG synthesis-related genes (p < 0.05). Moreover, TNFα KO presented a significantly increased expression of the FAO-related gene, CPT1, with a concomitant increase in the expression of glucose transporter 4 (GLUT4) and oxidative phosphorylation-related genes (CS and mt-CO1) (P < 0.05). Further evidence of the inhibition of fatty acid metabolism by TNFα includes a significant suppression of CPT1 as well as TG synthesis-related genes (P < 0.05) in 3T3-L1 adipocytes treated with TNFα. Conclusions These data indicate that antagonizing TNFα may mitigate diet-induced insulin resistance and hepatic steatosis by promoting FAO in obese AT. Funding Sources N/A.

scholarly journals High fat diet sensitizes fibromyalgia-like pain behaviors in mice via tumor necrosis factor alpha

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0190861 ◽  
Author(s):  
Dan Tian ◽  
Miao Tian ◽  
Leilei Zhang ◽  
Peng Zhao ◽  
Yunfeng Cui ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
High Fat Diet ◽  
Tumor Necrosis ◽  
High Fat ◽  
Necrosis Factor Alpha ◽  
Pain Behaviors ◽  
Factor Alpha ◽  
Necrosis Factor

Krill powder increases liver lipid catabolism and reduces glucose mobilization in tumor necrosis factor-alpha transgenic mice fed a high-fat diet

Metabolism ◽  
2012 ◽  
Vol 61 (10) ◽  
pp. 1461-1472 ◽  
Author(s):  
Bodil Bjørndal ◽  
Rita Vik ◽  
Trond Brattelid ◽  
Natalya Filipchuk Vigerust ◽  
Lena Burri ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Transgenic Mice ◽  
High Fat Diet ◽  
Tumor Necrosis ◽  
Liver Lipid ◽  
High Fat ◽  
Necrosis Factor Alpha ◽  
Lipid Catabolism ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Disruption of tumor necrosis factor alpha receptor 1 signaling accelerates NAFLD progression in mice upon a high-fat diet

2018 ◽  
Vol 58 ◽  
pp. 17-27 ◽  
Author(s):  
Flavia Lambertucci ◽  
Ainelén Arboatti ◽  
María Guillermina Sedlmeier ◽  
Omar Motiño ◽  
María de Luján Alvarez ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
High Fat Diet ◽  
Tumor Necrosis ◽  
High Fat ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Etanercept Ameliorates Cardiac Fibrosis in Rats with Diet-Induced Obesity

2021 ◽  
Vol 14 (4) ◽  
pp. 320
Author(s):  
Chia-Chen Hsu ◽  
Yingxiao Li ◽  
Chao-Tien Hsu ◽  
Juei-Tang Cheng ◽  
Mang Hung Lin ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Cardiac Fibrosis ◽  
Cardiac Injury ◽  
Vehicle Group ◽  
Necrosis Factor Alpha ◽  
Etanercept Treatment ◽  
Diet Induced Obesity ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Diet-induced obesity (DIO) is considered the main risk factor for cardiovascular diseases. Increases in the plasma levels of tumor necrosis factor alpha (TNF-α) is associated with DIO. Etanercept, a TNF-α inhibitor, has been shown to alleviate cardiac hypertrophy. To investigate the effect of etanercept on cardiac fibrosis in DIO model, rats on high fat diet (HFD) were subdivided into two groups: the etanercept group and vehicle group. Cardiac injury was identified by classic methods, while fibrosis was characterized by histological analysis of the hearts. Etanercept treatment at 0.8 mg/kg/week twice weekly by subcutaneous injection effectively alleviates the cardiac fibrosis in HFD-fed rats. STAT3 activation seems to be induced in parallel with fibrosis-related gene expression in the hearts of HFD-fed rats. Decreased STAT3 activation plays a role in the etanercept-treated animals. Moreover, fibrosis-related genes are activated by palmitate in parallel with STAT3 activation in H9c2 cells. Etanercept may inhibit the effects of palmitate, but it is less effective than a direct inhibitor of STAT3. Direct inhibition of STAT3 activation by etanercept seems unlikely. Etanercept has the ability to ameliorate cardiac fibrosis through reduction of STAT3 activation after the inhibition of TNF-α and/or its receptor.

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