Organelle dysfunction in hepatitis C virus-associated steatosis: anything to learn from nonalcoholic steatohepatitis?

Abstract

Nonalcoholic fatty liver disease (NAFLD) spans a pathological spectrum from nonalcoholic steatosis to steatohepatitis. The pathophysiology of this disorder is complex, but includes insulin resistance and disrupted lipid and carbohydrate homeostasis, which at a subcellular level results in oxidative stress, free fatty acid-mediated lipotoxicity, defects in mitochondrial function, endoplasmic reticulum stress and cytokine-mediated toxicity. In chronic hepatitis C (CHC), systemic metabolic derangements similar to NAFLD may be operative, but in addition, virus-specific factors contribute to steatosis. The mechanisms for steatosis in CHC appear to share common pathways with those observed in NAFLD. This article outlines our current understanding of the subcellular mechanisms of steatosis in NAFLD and CHC, including their similarities and differences.

Independent association between low serum amylase and non-alcoholic fatty liver disease in asymptomatic adults: a cross-sectional observational study

“…Low prevalence rates of hepatitis C (<1.5%) were also recently reported in Asian-Pacific, tropical Latin American and North American countries 52. Therefore, hepatitis C infection is unlikely to profoundly modify the association between LSA and NAFLD in this study, although hepatitis C infection can contribute to the development of NAFLD 53. It is also possible that individuals with primary biliary cirrhosis, autoimmune hepatitis or other forms of liver dysfunction (eg, haemochromatosis and Wilson disease) were included in the present study, even though we excluded subjects with elevated hepatic enzymes (≥150 IU/ml).…”

Hepatitis C Virus Infection, Metabolic Disorders and Non-alcoholic Fatty Liver Disease: A Literature Review

“…Nonetheless, other factors including HCV-induced metabolic syndrome have also been implicated as significant factors [19]. In molecular levels, Shlomai et al [20] have suggested that the metabolic regulator peroxisome proliferatoractivated receptor-gamma co-activator 1α is strongly induced following HCV infection, resulting in an upregulated gluconeogenic response; This observation provides evidence for a linkage between HCV infection and hepatic insulin resistance. In cellular level, HCV infection has been suggested to induce organelle dysfunction which leads to the development of NAFLD [21].…”

Perspectives on cellular dysfunction in nonalcoholic steatohepatitis: a case of ‘multiorganelle failure’? Proceedings of a virtual workshop on nonalcoholic steatohepatitis

“…To this end, the lessons from common steatogenic conditions such as NAFLD and hepatitis C virus infection may well be interchangeable [27,28]. Chronic viral hepatitis C will tend to improve histo logically once the hepatitis C virus is eradicated by successful antiviral regimens.…”