Location of Repository

Hepatitis C and insulin resistance: steatosis, fibrosis and non-response Hepatitis C y resistencia a la insulina: esteatosis, fibrosis y no respuesta

By M. Romero-Gómez

Abstract

Insulin resistance is more often seen in hepatitis C than in other liver diseases, including non-alcoholic steatohepatitis. The Homeostasis Model for Assessment [HOMA= fasting insulin (mUI/ml) * fasting glucose (mmol/L) / 22.5] has proved useful in the measurement of insulin sensitivity in euglycemic patients. Cross-sectional and case-cohort studies support a role for hepatitis C as a factor implied in the development of type-2 diabetes in high-risk patients (male patients, older than 40 years, and overweight). In transgenic mice models the HCV core protein has been found to induce insulin resistance via TNF production. Insulin resistance has been associated with steatosis development and fibrosis progression in a genotype-dependent manner. In genotype-1 patients, the mechanisms by which insulin resistance promotes fibrosis progression include: a) steatosis; b) hyperleptinemia; c) increased TNF production; and d) impaired expression of PPARγ receptors. Indeed, insulin resistance has been found as a common denominator to the majority of features associated with difficult-to-treat patients. Patients with cirrhosis, obesity, coinfected with HIV, and Afro-American, all of them showed insulin resistance. Insulin resistance strongly influences sustained response rates, at least in genotype-1 patients. Insulin resistance decreases during and after treatment in patients that achieved virus C clearance. Moreover, the incidence of type-2 diabetes seems to be lower in responders than in non-responders. In summary, hepatitis C promotes insulin resistance and insulin resistance induces steatosis, fibrosis, and interferon resistance. The treatment of insulin resistance by decreasing hyperinsulinemia could improve sustained response rates in patients with chronic hepatitis C treated with peginterferon plus ribavirin

Topics: Hepatitis C, Insulin resistance, Steatosis, Fibrosis, Internal medicine, RC31-1245, Medicine, R, DOAJ:Internal medicine, DOAJ:Medicine (General), DOAJ:Health Sciences, Diseases of the digestive system. Gastroenterology, RC799-869, Specialties of internal medicine, RC581-951, DOAJ:Gastroenterology
Publisher: Aran Ediciones
Year: 2006
OAI identifier: oai:doaj.org/article:06e540e87cf1405394543260410a8fa6
Journal:
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • https://doaj.org/toc/1130-0108 (external link)
  • http://scielo.isciii.es/scielo... (external link)
  • https://doaj.org/article/06e54... (external link)
  • Suggested articles


    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.