ArticleThe Journal of biological chemistry2017
Hepatitis C virus induces a prediabetic state by directly impairing hepatic glucose metabolism in mice.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- A novel variant of fructose-1,6-bisphosphatase gene identified in an adult with newly diagnosed hepatitis C.JIMD reports · 2022Article
- A maternal high-fat/low-fiber diet impairs glucose tolerance and induces the formation of glycolytic muscle fibers in neonatal offspring.European journal of nutrition · 2021Article
- Hepatocrinology.Medical sciences (Basel, Switzerland) · 2021Review
- Metabolic complications of hepatitis C virus infection.World journal of gastroenterology · 2021Review
- Glycogen synthase kinase (GSK)-3 and the double-strand RNA-dependent kinase, PKR: When two kinases for the common good turn bad.Biochimica et biophysica acta. Molecular cell research · 2020Review
- The Constitutive Lack of α7 Nicotinic Receptor Leads to Metabolic Disorders in Mouse.Biomolecules · 2020Article
- Natural History of Hepatic and Extrahepatic Hepatitis C Virus Diseases and Impact of Interferon-Free HCV Therapy.Cold Spring Harbor perspectives in medicine · 2020Review
- Review
- New roles for prokineticin 2 in feeding behavior, insulin resistance and type 2 diabetes: Studies in mice and humans.Molecular metabolism · 2019Article
- Non-Targeted UHPLC-Q-TOF/MS-Based Metabolomics Reveals a Metabolic Shift from Glucose to Glutamine in CPB Cells during ISKNV Infection Cycle.Metabolites · 2019Article
- Cellular Stresses and Stress Responses in the Pathogenesis of Insulin Resistance.Oxidative medicine and cellular longevity · 2018Review
- Robust Regression Analysis of GCMS Data Reveals Differential Rewiring of Metabolic Networks in Hepatitis B and C Patients.Metabolites · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Virus-related type 2 diabetes is commonly observed in individuals infected with the hepatitis C virus (HCV); however, the underlying molecular mechanisms remain unknown. Our aim was to unravel these mechanisms using FL-N/35 transgenic mice expressing the full HCV ORF. We observed that these mice displayed glucose intolerance and insulin resistance. We also found that Glut-2 membrane expression was reduced in FL-N/35 mice and that hepatocyte glucose uptake was perturbed, partly accounting for the HCV-induced glucose intolerance in these mice. Early steps of the hepatic insulin signaling pathway, from IRS2 to PDK1 phosphorylation, were constitutively impaired in FL-N/35 primary hepatocytes via deregulation of TNFα/SOCS3. Higher hepatic glucose production was observed in the HCV mice, despite higher fasting insulinemia, concomitant with decreased expression of hepatic gluconeogenic genes. Akt kinase activity was higher in HCV mice than in WT mice, but Akt-dependent phosphorylation of the forkhead transcription factor FoxO1 at serine 256, which triggers its nuclear exclusion, was lower in HCV mouse livers. These findings indicate an uncoupling of the canonical Akt/FoxO1 pathway in HCV protein-expressing hepatocytes. Thus, the expression of HCV proteins in the liver is sufficient to induce insulin resistance by impairing insulin signaling and glucose uptake. In conclusion, we observed a complete set of events leading to a prediabetic state in HCV-transgenic mice, providing a valuable mechanistic explanation for HCV-induced diabetes in humans.
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