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Endogenous CSE/H 2 S system mediates TNF‐α‐induced insulin resistance in 3T3‐L1 adipocytes
Author(s) -
Huang CiYou,
Yao WeiFeng,
Wu Weiguo,
Lu YuLian,
Wan Hui,
Wang Wen
Publication year - 2013
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.2920
Subject(s) - insulin resistance , endogeny , 3t3 l1 , endocrinology , insulin , medicine , tumor necrosis factor alpha , downregulation and upregulation , adipocyte , glucose uptake , type 2 diabetes , chemistry , diabetes mellitus , biology , adipose tissue , biochemistry , gene
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.