Involvement of CSE/ H2S in high glucose induced aberrant secretion of adipokines in 3T3-L1 adipocytes

Lipids in Health and Disease

Research

Zhe Pan¹  Hanbo Wang² 

[1] Department of Endocrinology, Shandong Provincial Hospital affiliated to Shandong University; Shandong Clinical Medical Center of Endocrinology and Metabolism; Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, 324 Jing 5 Rd, 250021, Jinan, Shandong, P. R. China;Minimally Invasive Urology Center, Shandong Provincial Hospital affiliated to Shandong University, 250021, Jinan, China;

关键词: High glucose;    Cystathionine-γ-lyase;    HS;    Adipokine;    Adipocyte;   

DOI  :  10.1186/1476-511X-13-155

 received in 2014-06-29, accepted in 2014-09-28,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundDeregulated secretion of adipokines contributes to subclinical systemic inflammation associated with type 2 diabetes mellitus (T2DM). However, the mechanisms underlying are not fully understood. Hydrogen sulfide (H2S), as an endogenous gasotransmitter, possesses an anti-inflammation activity. The aim of this study was to examine the possible involvement of H2S in high glucose induced adipokine secretion in 3T3-L1 adipocytes.MethodsThe expression of cystathionine-gamma-lyase (CSE), the H2S-forming enzyme, was evaluated by Western-blotting and real-time PCR. The secretion of TNF-α, MCP-1 and adiponectin was determined by radioimmunoassay and enzyme-linked immunosorbent assay (ELISA), respectively. Lentiviral empty vector and vector expressing mouse CSE were used for in vitro transduction.ResultsHigh glucose (HG) significantly decreased CSE expression at both protein and mRNA levels in mature 3T3-L1 adipocytes. In parallel, HG significantly increased secretion of MCP-1 while decreasing secretion of adiponectin, but had no effect on secretion of TNF-α. HG induced changes in MCP-1 and adiponectin secretion were partly attenuated by forced expression of CSE or sodium hydrosulfide (NaHS), a source of exogenous H2S.ConclusionHigh glucose induces aberrant secretion of adipokines in mature 3T3-L1 adipocytes, favoring inflammation. The mechanism is partly related to inhibition of CSE/ H2S system.

【 授权许可】

Unknown   
© Pan et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.