Fructose and glucose can regulate mammalian target of rapamycin complex 1 and lipogenic gene expression via distinct pathways.
Fiche publication
Date publication
février 2018
Journal
The Journal of biological chemistry
Auteurs
Membres identifiés du Cancéropôle Est :
Pr MASSON David
Tous les auteurs :
Hu Y, Semova I, Sun X, Kang H, Chahar S, Hollenberg AN, Masson D, Hirschey MD, Miao J, Biddinger SB
Lien Pubmed
Résumé
Although calorically equivalent to glucose, fructose appears to be more lipogenic, promoting dyslipidemia, fatty liver disease, cardiovascular disease, and diabetes. To better understand how fructose induces lipogenesis, we compared the effects of fructose and glucose on mammalian target of rapamycin complex 1 (mTORC1), which appeared to have both positive and negative effects on lipogenic gene expression. We found that fructose acutely and transiently suppressed mTORC1 signaling and The constitutive activation of mTORC1 reduced hepatic lipogenic gene expression and produced hypotriglyceridemia after 1 week of fructose feeding. In contrast, glucose did not suppress mTORC1, and the constitutive activation of mTORC1 failed to suppress plasma triglycerides after 1 week of glucose feeding. Thus, these data reveal fundamental differences in the signaling pathways used by fructose and glucose to regulate lipid metabolism.
Mots clés
dyslipidemia, fructose, glucose, lipogenesis, mammalian target of rapamycin (mTOR), metabolic syndrome
Référence
J. Biol. Chem.. 2018 Feb 9;293(6):2006-2014