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Fructose and glucose regulate mammalian target of rapamycin complex 1 and can activate lipogenic gene expression via distinct pathways.

Fructose and glucose regulate mammalian target of rapamycin complex 1 and can activate lipogenic gene expression via distinct pathways.
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Hu Y, Semova I, Sun X, Kang H, Chahar S, Hollenberg AN, Masson D, Hirschey MD, Miao J, Biddinger SB,


Hu Y, Semova I, Sun X, Kang H, Chahar S, Hollenberg AN, Masson D, Hirschey MD, Miao J, Biddinger SB, (click to view)

Hu Y, Semova I, Sun X, Kang H, Chahar S, Hollenberg AN, Masson D, Hirschey MD, Miao J, Biddinger SB,

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The Journal of biological chemistry 2017 12 08() pii jbc.M117.782557
Abstract

Though calorically equivalent to glucose, fructose appears to be more lipogenic, leading to dyslipidemia, fatty liver disease, cardiovascular disease, and diabetes. To better understand how fructose induces lipogenesis, we compared the effects of fructose and glucose on the mTORC1 signaling node, a central regulator of lipogenesis. We found that fructose acutely and transiently suppressed mTORC1 signaling in vitro and in vivo. The constitutive activation of mTORC1 reduced hepatic lipogenic gene expression and produced hypotriglyceridemia after one week of fructose feeding. In contrast, glucose did not inhibit mTORC1, and constitutive activation of mTORC1 failed to suppress either lipogenic gene expression or plasma triglycerides after one week of glucose feeding. Taken together, these data reveal differences in the interactions of glucose and fructose with the mTORC1 signaling node.

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