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. 2015 Sep 14;6:134. doi: 10.3389/fendo.2015.00134

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Copyright © 2015 Hammerstad, Grock, Lee, Hasham, Sundaram and Tomer.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential mechanisms by which HCV directly affects the insulin signaling cascade. HCV infection of liver cells can lead to (1) decreased insulin receptor (IR in the figure) auto phosphorylation; (2) decreased IRS-1 activation due to increased serine-phosphorylation of IRS-1; (3) decreased IRS-1 levels due to increased ubiquitin-mediated proteasomal degradation induced by SOCS 3/7 and mTOR upregulation; (4) reduced Akt activity due to increased threonine-phosphorylation of Akt; (5) decreased GLUT4 expression; and (6) increased gluconeogenic enzymes (GC6P and PCK2). IR, insulin receptor; IRS-1, insulin receptor substrate-1; SOCS 3/7, suppressor of cytokine signaling; PI3K, phosphoinositide 3-kinase; mTOR, mammalian target of rapamycin; GC6P, glucose-6-phosphatase; PCK2, phosphoenolpyruvate carboxykinase 2.