Abstract
Chronic Hepatitis C virus has the potential of inducing insulin resistance and type 2 Diabetes Mellitus in vitro as well as in vivo . Structural and non-structural proteins of HCV modulate cellular gene expression in such a way that insulin signaling is hampered, concomitantly leads toward diabetes mellitus. A number of mechanisms have been proposed in regard to the HCV induced insulin resistance involving the upregulation of Inflammatory cytokine TNF-α, hypophosphorylation of IRS-1 and IRS-2, phosphorylation of Akt, up-regulation of gluconeogenic genes, accumulation of lipids and targeting lipid storage organelles. This review provides an insight of molecular mechanisms by which HCV structural and non-structural proteins can induce insulin resistance.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Diabetes Mellitus, Type 2 / etiology
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Diabetes Mellitus, Type 2 / metabolism*
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Diabetes Mellitus, Type 2 / physiopathology
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Diabetes Mellitus, Type 2 / virology
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Gene Expression Regulation*
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Gluconeogenesis
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Glucose / metabolism
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Hepacivirus / genetics
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Hepacivirus / metabolism*
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Hepatitis C, Chronic / complications
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Hepatitis C, Chronic / metabolism*
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Hepatitis C, Chronic / physiopathology
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Hepatitis C, Chronic / virology
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Humans
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Insulin / metabolism
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Insulin Receptor Substrate Proteins / genetics
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Insulin Receptor Substrate Proteins / metabolism
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Insulin Resistance*
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Lipogenesis
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Mice
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Mice, Transgenic
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Phosphorylation
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism
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Signal Transduction*
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Tumor Necrosis Factor-alpha / biosynthesis
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Viral Nonstructural Proteins / genetics
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Viral Nonstructural Proteins / metabolism*
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Viral Structural Proteins / genetics
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Viral Structural Proteins / metabolism*
Substances
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Insulin
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Insulin Receptor Substrate Proteins
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Tumor Necrosis Factor-alpha
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Viral Nonstructural Proteins
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Viral Structural Proteins
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Proto-Oncogene Proteins c-akt
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Glucose