Hydrogen sulfide protects against high glucose-induced lipid metabolic disturbances in 3T3-L1 adipocytes via the AMPK signaling pathway

Aberrant lipid metabolism contributes to the development of type 2 diabetes mellitus. The mechanisms by which hydrogen sulfide (H(2)S), an endogenous gasotransmitter, regulates lipid metabolism remain unclear. The aim of the present study was to investigate if the protective effects of H(2)S during high glucose (HG)-induced lipid accumulation in 3T3-L1 adipocytes may be mediated by AMP-activated protein kinase (AMPK). Triglyceride (TG) content and the production of H(2)S were determined using adipogenesis colorimetric assay kits and H(2)S synthesis methods. The levels of monocyte chemoattractant protein-1 and adiponectin were evaluated by ELISA. Total AMPK and phosphorylated AMPK levels were assessed by western blot analysis. HG increased the cellular level of TG and decreased H(2)S production in 3T3-L1 adipocytes. The H(2)S donor, sodium hydrosulfide (NaHS) protected against the HG-induced accumulation of TG in 3T3-L1 adipocytes. Furthermore, NaHS suppressed HG-induced TG accumulation by activating AMPK. Collectively, the findings of the present study suggested that HG induced lipid accumulation in 3T3-L1 adipocytes, and AMPK activation may underlie the lipid-lowering effects of H(2)S.