Published online Jan 28, 2016. doi: 10.3748/wjg.v22.i4.1461
Peer-review started: June 4, 2015
First decision: July 14, 2015
Revised: August 14, 2015
Accepted: October 23, 2015
Article in press: October 26, 2015
Published online: January 28, 2016
In addition to causing cirrhosis and hepatocellular carcinoma, hepatitis C virus (HCV) is thought to cause hypolipidemia, hepatic steatosis, insulin resistance, metabolic syndrome, and diabetes. The viral life cycle of HCV depends on cholesterol metabolism in host cells. HCV core protein and nonstructural protein 5A perturb crucial lipid and glucose pathways, such as the sterol regulatory element-binding protein pathway and the protein kinase B/mammalian target of rapamycin/S6 kinase 1 pathway. Although several lines of transgenic mice expressing core or full HCV proteins exhibit hepatic steatosis and/or dyslipidemia, whether they completely reflect the metabolic alterations in humans with HCV infection remains unknown. Many cross-sectional studies have demonstrated increased prevalences of metabolic alterations and cardiovascular events in patients with chronic hepatitis C (CHC); however, conflicting results exist, primarily due to unavoidable individual variations. Utilizing anti-HCV therapy, most longitudinal cohort studies of CHC patients have demonstrated the favorable effects of viral clearance in attenuating metabolic alterations and cardiovascular risks. To determine the risks of HCV-associated metabolic alterations and associated complications in patients with CHC, it is necessary to adjust for crucial confounders, such as HCV genotype and host baseline glucose metabolism, for a long follow-up period after anti-HCV treatment. Adipose tissue is an important endocrine organ due to its release of adipocytokines, which regulate lipid and glucose metabolism. However, most data on HCV infection and adipocytokine alteration are inconclusive. A comprehensive overview of HCV-associated metabolic and adipocytokine alterations, from bench to bedside, is presented in this topic highlight.
Core tip: Hepatitis C virus (HCV) is thought to cause hypolipidemia, hepatic steatosis, insulin resistance, and diabetes. Its life cycle depends on host cholesterol metabolism. HCV core protein and nonstructural protein 5A perturb crucial metabolic pathways. Many cross-sectional studies have demonstrated increased cardiometabolic risks in HCV patients. Utilizing anti-HCV therapy, most cohort studies have demonstrated the favorable effects of HCV clearance in attenuating cardiometabolic risks. Adipose tissue is an important endocrine organ due to its release of adipocytokines, which strongly regulate metabolism. A comprehensive overview of HCV-associated metabolic and adipocytokine alterations, from bench to bedside, is presented in this topic highlight.