Abstract
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.
Highlights
Deregulated secretion of adipokines contributes to subclinical systemic inflammation associated with type 2 diabetes mellitus (T2DM)
We investigated the potential role of CSE/ H2S system in regulation of adipokine secretion in 3T3-L1 adipocytes under high glucose condition
High glucose downregulated CSE protein expression in 3T3-LI preadipocytes and adipocytes In our previous study, we demonstrated that HG downregulated CSE expression in HUVEC cells [14]
Summary
Deregulated secretion of adipokines contributes to subclinical systemic inflammation associated with type 2 diabetes mellitus (T2DM). Hydrogen sulfide (H2S), as an endogenous gasotransmitter, possesses an anti-inflammation activity. The mechanisms that govern the association between T2DM and the increased synthesis of inflammatory factors are not fully understood. Hydrogen sulfide (H2S) is a lately identified endogenous gasotransmitter. The generation of H2S in mammalian tissues is catalyzed by two major enzymes, cystathionineβ-synthase (CBS) and cystathionine-γ-lyase (CSE). Both are pyroxidal-5′-phosphate dependent enzymes that use L-cysteine and homocysteine as substrates [5,6] A third H2S synthesizing enzyme is 3-mercaptopyruvate sulfur transferase (3MST), which utilizes L-cysteine and αketoglutarate to produce H2S [7]. CSE is the principal H2S-forming enzyme in the vasculature and heart, whereas CBS and 3MST are most abundantly expressed in the central nervous system
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