scholarly journals Influence of iron sulfate on adipose tissue endocrine dysfunction in Wistar rats

2013 ◽  
Vol 94 (5) ◽  
pp. 760-763
Author(s):  
A A Tinkov ◽  
E V Popova ◽  
A A Nikonorov

Aim. To study the adipose tissue endocrine function at adipogenic effect development in Wistar rats on high-fat diet and increased iron intake with drinking water. Methods. Animals on standard and high-fat diets were administered 3 mg/l of iron sulfate with drinking water during 3 months. Levels of circulating proinflammatory cytokines (monocyte chemoattractant protein 1, tumor necrosis factor alpha), leptin, adiponectin, serum glucose and insulin, as well as morphometric parameters and iron content in hair and adipose tissue were evaluated. Results. A significant increase in morphometric parameters, hair iron levels was observed in rats taking iron salts compared to the controls, with highest adipose tissue iron level in rats on high-fat diet. At the same time, serum levels of proinflammatory cytokines (monocyte chemoattractant protein 1, tumor necrosis factor alpha) and leptin was also higher in rats obtaining iron with drinking water compared to controls. Increased serum insulin level together with slightly elevated serum glucose level indicated insulin resistance development in rats on high-fat diet, fed with iron. Conclusion. The research shows that, on the one side, iron intake potentiates the adipogenic effect of high-fat diet, and on the other side, acting as a trigger for endocrine dysfunction formation (so called endocrine disruptor).

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0190861 ◽  
Author(s):  
Dan Tian ◽  
Miao Tian ◽  
Leilei Zhang ◽  
Peng Zhao ◽  
Yunfeng Cui ◽  
...  

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1705-1705
Author(s):  
Seok-Yeong Yu ◽  
Jinchao Li ◽  
Zhenhua Liu ◽  
Young-Cheul Kim

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.


2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Ran Meng ◽  
Da-Long Zhu ◽  
Yan Bi ◽  
Dong-Hui Yang ◽  
Ya-Ping Wang

We investigated the effects of apocynin on high-fat diet- (HFD-) induced insulin resistance in C57BL/6 mice. After 12 weeks of HFD, the mice that exhibited insulin resistance then received 5 weeks of apocynin (2.4 g/L, in water). Following apocynin treatment, fasting glucose, insulin, and glucose tolerance test showed significant improvement in insulin sensitivity in HFD-fed mice. We demonstrated that serum levels of tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6), and leptin were remarkably reduced with apocynin treatment. We also found that mRNA expression of TNF-α, IL-6, and monocyte chemoattractant protein-1 (MCP-1) in the liver and mRNA expression of TNF-α, IL-6, MCP-1, and leptin in adipose tissue were suppressed by apocynin. Furthermore, the activity of transcription factor NF-κB in the liver was significantly suppressed with apocynin treatment. These results suggest that apocynin may reduce inflammatory factors in the blood, liver, and adipose tissue, resulting in amelioration of insulin resistance in HFD-fed mice.


Metabolism ◽  
2012 ◽  
Vol 61 (10) ◽  
pp. 1461-1472 ◽  
Author(s):  
Bodil Bjørndal ◽  
Rita Vik ◽  
Trond Brattelid ◽  
Natalya Filipchuk Vigerust ◽  
Lena Burri ◽  
...  

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