Editorial
Copyright ©2009 The WJG Press and Baishideng.
World J Gastroenterol. Oct 28, 2009; 15(40): 4993-4999
Published online Oct 28, 2009. doi: 10.3748/wjg.15.4993
Figure 1
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Figure 1 HCV-induced insulin resistance. Dotted lines represent inhibition, continuous lines represent activation. PI3K: Phosphatidyl-inositol 3 kinase.
Figure 2
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Figure 2 HCV-induced insulin resistance[21-23]. SOC-3: Suppressor of cytokine-3; PPAR: Peroxisome proliferators activated receptor; HSCs: Hepatic stellate cells.
Figure 3
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Figure 3 Core-protein induced insulin resistance[21-23].
Figure 4
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Figure 4 Insulin-induced IFN resistance. Interaction between insulin and the PEG-interferon α-signaling pathway. PI3K activated by insulin seems to be responsible for the block of STAT1 translocation that avoids the antiviral effect of interferon. Dotted lines represent inhibition, continuous lines represent activation. IRS-2: Insulin substrate-2; 2',5'-OAS: 2',5'-oligoadenylate synthetase; PKR: Protein kinase.