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Direct Hepatocyte Insulin Signaling Is Required for Lipogenesis but Is Dispensable for the Suppression of Glucose Production
Insulin's direct action on liver cells is needed to make fat but not to reduce glucose production
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Abstract
Insulin-resistant states such as type II diabetes mellitus (T2DM) show that insulin promotes lipid synthesis while failing to suppress hepatic glucose production.
- Akt-dependent activation of mTORC1 and inhibition of Foxo1 are needed for the production of new fatty acids in the liver.
- Hepatic insulin signaling may remain functional during insulin resistance, contrary to expectations.
- Insulin's ability to lower glucose production in the liver is influenced by a decrease in fat breakdown in fat cells and levels of free fatty acids in the blood.
- This suppression of glucose production does not rely on signals from the vagus nerve or glucagon.
- Excess free fatty acids in circulation may contribute to the inability to suppress glucose production in T2DM.
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