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Quinine is a bitter tasting compound that is involved in the regulation of body weight as demonstrated in  in vivo  animal models and  in vitro  models of the adipogenic system. Arguments exist over the positive or negative roles of quinine in both  in vivo  animal models and  in vitro  cell models, which motivates us to further investigate the functions of quinine in the  in vitro  adipogenic system. To clarify the regulatory functions of quinine in adipogenesis, mouse primary preadipocytes were induced for differentiation with quinine supplementation. The results showed that quinine enhanced adipogenesis in a dose dependent manner without affecting lipolysis. The pro-adipogenic effect of quinine was specific, as other bitter tasting agonists had no effect on adipogenesis. Moreover, the pro-adipogenic effect of quinine was mediated by activation of ERK/S6 (extracellular-signal-regulated kinase/Ribosomal protein S6) signaling. Knockdown of bitter taste receptor T2R106 (taste receptor, type 2, member 106) impaired the pro-adipogenic effect of quinine and suppressed the activation of ERK/S6 signaling. Taken together, quinine stimulates adipogenesis through ERK/S6 signaling, which at least partly functions via T2R106.

Regulation of Adipogenesis by Quinine through the ERK/S6 Pathway