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Int. J. Mol. Sci. 2016, 17(4), 504;

Regulation of Adipogenesis by Quinine through the ERK/S6 Pathway

Laboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest Agriculture and Forestry University, Yangling 712100, China
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Toshiro Arai
Received: 22 February 2016 / Revised: 24 March 2016 / Accepted: 29 March 2016 / Published: 13 April 2016
(This article belongs to the Special Issue Molecular Research on Obesity and Diabetes)
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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. View Full-Text
Keywords: quinine; adipogenesis; T2R106; ERK/S6 signaling quinine; adipogenesis; T2R106; ERK/S6 signaling

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Ning, X.; He, J.; Shi, X.; Yang, G. Regulation of Adipogenesis by Quinine through the ERK/S6 Pathway. Int. J. Mol. Sci. 2016, 17, 504.

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