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Aydin Yildirim T, Kitis Y
The primary function of hepatic insulin signaling is to decrease HGP by repressing gluconeogenesis mediated by the Akt-induced phosphorylation of forkhead box O1 (FOXO1) [15], which excludes FOXO1 from the nucleus, and thus, prevents the transcriptional activations of gluconeogenic gene expressions, such as glucose-6-phosphatase (G6PC) and phosphoenolpyruvate carboxylase (PEPCK) [15,16]
e., hyperglucagonemia) is observed 1, 4,5,6 , suggesting the regulation of glucagon secretion is impaired
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