NDLI: Endogenous $CSE/H_{2}S$ system mediates TNF-α-induced insulin resistance in 3T3-L1 adipocytes

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Endogenous $CSE/H_{2}S$ system mediates TNF-α-induced insulin resistance in 3T3-L1 adipocytes

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Huang, Ci-You Yao, Wei-Feng Wu, Wei-guo Lu, Yu-Lian Wan, Hui Wang, Wen
Description	Country affiliation: China Author Affiliation: Huang CY ( Department of Endocrinology, Affiliated Wuxi Second Hospital, Nanjing Medical University, Wuxi, 214002, Jiangsu, China. wxhuangcy@163.com)
Abstract	Tumour necrosis factor-α (TNF- α)is a major contributor to the pathogenesis of insulin resistance associated with obesity and type 2 diabetes. It has been found that endogenous hydrogen sulfide $(H_{2}S)$ contributes to the pathogenesis of diabetes. We have hypothesized that TNF-α-induced insulin resistance is involved in endogenous $H_{2}S$ generation. The aim of the present study is to investigate the role of endogenous $H_{2}S$ in TNF-α-induced insulin resistance by studying 3T3-L1 adipocytes. We found that treatment of 3T3-L1 adipocytes with TNF-α leads to deficiency in insulin-stimulated glucose consumption and uptake and increase in endogenous $H_{2}S$ generation. We show that cystathionine γ-lyase (CSE) is catalysed in 3T3-L1 adipocytes to generate $H_{2}S$ and that CSE expression and activity are upregulated by TNF-α treatment. Inhibited CSE by its potent inhibitors significantly attenuates TNF-α-induced insulin resistance in 3T3-L1 adipocytes, whereas $H_{2}S$ treatment of 3T3-L1 adipocytes impairs insulin-stimulated glucose consumption and uptake. These data indicate that endogenous $CSE/H_{2}S$ system contributes to TNF-α-caused insulin resistance in 3T3-L1 adipocytes. Our findings suggest that modulation of $CSE/H_{2}S$ system is a potential therapeutic avenue for insulin resistance. Copyright © 2012 John Wiley & Sons, Ltd.
File Format	HTM / HTML
ISSN	02636484
Issue Number	6
Volume Number	31
e-ISSN	10990844
Journal	Cell Biochemistry and Function
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2013-08-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Cell Biology Discipline Biochemistry Cystathionine Gamma-lyase Metabolism Diabetes Mellitus, Type 2 Hydrogen Sulfide Insulin Resistance Genetics Obesity Tumor Necrosis Factor-alpha 3t3-l1 Cells Adipocytes Animals Pathology Glucose Humans Insulin Mice Journal Article Research Support, Non-u.s. Gov't
Alternative Title	Endogenous CSE/H2 S system mediates TNF- -induced insulin resistance in 3T3-L1 adipocytes
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Biochemistry Clinical Biochemistry

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Tumor Necrosis Factor (TNF)-α-induced Repression of GKAP42 Protein Levels through cGMP-dependent Kinase (cGK)-Iα Causes Insulin Resistance in 3T3-L1 Adipocytes

Cystathionine γ lyase–hydrogen sulfide increases peroxisome proliferator-activated receptor γ activity by sulfhydration at C139 site thereby promoting glucose uptake and lipid storage in adipocytes

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Endogenous $CSE/H_{2}S$ system mediates TNF-α-induced insulin resistance in 3T3-L1 adipocytes

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