Hydrogen sulfide impacts on inflammation-induced adipocyte dysfunction.

A dual role of hydrogen sulfide (HS) in inflammation is well-reported and recent studies demonstrated adipogenic effects of HS in 3T3-L1 cells. Here, we aimed to investigate the effects of HS on adipocyte differentiation and inflammation. HS concentration in 3T3-L1 culture media was increased during adipocyte differentiation in parallel to adipogenic and Cth gene expression, and its inhibition using DL-Propargyl Glycine (PPG) impaired 3T3-L1 differentiation. GYY4137 and NaS administration only in the first or in the last stage of adipocyte differentiation resulted in a significant increased expression of adipogenic genes. However, when GYY4137 or NaS were administrated during all process no significant effects on adipogenic gene expression were found, suggesting that excessive HS administration might exert negative effects on adipogenesis. In fact, continuous addition of NaS, which resulted in NaS excess, inhibited adipogenesis, whereas time-expired NaS had no effect. In inflammatory conditions, GYY4137, but not NaS, administration attenuated the negative effects of inflammation on adipogenesis and insulin signaling-related gene expression during adipocyte differentiation. In inflamed adipocytes, NaS administration enhanced the negative effects of inflammatory process. Altogether these data showed that slow-releasing HS improved adipocyte differentiation in inflammatory conditions, and that HS proadipogenic effects depend on dose, donor and exposure time.