Capsaicin Targets Lipogenesis in HepG2 Cells Through AMPK Activation, AKT Inhibition and PPARs Regulation
AuthorBort Bueno, Alicia Carmen; Sánchez Gómez, Belén; Mateos Gómez, Pedro Antonio; Díaz-Laviada Marturet, Inés; Rodríguez Henche, Nieves
IdentifiersEnlace permanente (URI): http://hdl.handle.net/10017/37531
Fundación Tatiana Pérez De Guzmán
International Journal of Molecular Sciences, 2019, v. 20(7), n. 1660, p. -
FUNDACIÓN TATIANA PÉREZ DE GUZMÁN, grant Patrocinio 2013-001 and grant Patrocinio 2019-001.
Tipo de documento
Attribution 4.0 International (CC BY 4.0)
© 2019 The Author(s)
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Obesity, a major risk factor for chronic diseases such as type 2 diabetes (T2D), represents a serious primary health problem worldwide. Dietary habits are of special interest to prevent and counteract the obesity and its associated metabolic disorders, including lipid steatosis. Capsaicin, a pungent compound of chili peppers, has been found to ameliorate diet-induced obesity in rodents and humans. The purpose of this study was to examine the effect of capsaicin on hepatic lipogenesis and to delineate the underlying signaling pathways involved, using HepG2 cells as an experimental model. Cellular neutral lipids, stained with BODIPY493/503, were quantified by flow cytometry, and the protein expression and activity were determined by immunoblotting. Capsaicin reduced basal neutral lipid content in HepG2 cells, as well that induced by troglitazone or by oleic acid. This effect of capsaicin was prevented by dorsomorphin and GW9662, pharmacological inhibitors of AMPK and PPARgamma, respectively. In addition, capsaicin activated AMPK and inhibited the AKT/mTOR pathway, major regulators of hepatic lipogenesis. Furthermore, capsaicin blocked autophagy and increased PGC-1alfa protein. These results suggest that capsaicin behaves as an anti-lipogenic compound in HepG2 cells.
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