Abstract
BackgroundHepatic steatosis is often seen in patients with chronic hepatitis C (CH-C). It is still unclear whether these patients have an impaired mitochondrial β-oxidation. In this study we assessed mitochondrial β-oxidation in CH-C patients by investigating ketogenesis during fasting.MethodsThis study consisted of thirty patients with CH-C. Serum levels of insulin and hepatitis C virus (HCV) core protein were measured by chemiluminescence enzyme immunoassay. The subjects were then fasted, and venous blood samples were drawn 12 h and 15 h after the start of fasting. The levels of blood ketone bodies were measured by an enzymatic cycling method. The rate of change in total ketone body concentration was compared with that in eight healthy volunteers.ResultsThe rate of change in total ketone body concentration between 12 h and 15 h after the start of fasting was significantly lower in CH-C patients than in healthy volunteers (129.9% (8.5-577.3%) vs. 321.6% (139.6-405.4%); P <0.01). The rate of change in total ketone body concentration in patients with a serum level of HCV core protein of 10000 fmol/L or higher was significantly lower than in patients with a level of less than 10000 fmol/L (54.8% (8.5-304.3%) vs. 153.6% (17.1-577.3%); P <0.05). The rate of change in total ketone body concentration in patients with a homeostasis model assessment of insulin resistance (HOMA-IR) of 2.5 or higher was significantly lower than in patients with a HOMA-IR of less than 2.5 (56.7% (8.5-186.7%) vs. 156.4% (33.3-577.3%); P <0.01).ConclusionsThese results suggest that mitochondrial β-oxidation is impaired, possibly due to HCV infection in patients with CH-C.
Highlights
Hepatic steatosis is often seen in patients with chronic hepatitis C (CH-C)
The results of our study suggest that mitochondrial βoxidation is impaired, possibly due to Hepatitis C virus (HCV) infection
Further studies are needed to elucidate the detailed pathophysiology of impaired fatty acid metabolism in CH-C and its clinical significance
Summary
Hepatic steatosis is often seen in patients with chronic hepatitis C (CH-C). It is still unclear whether these patients have an impaired mitochondrial β-oxidation. Hepatitis C virus (HCV) infection is a major cause of chronic liver injury. Hepatic steatosis is one of histologic features of chronic HCV infection with a risk of progression of liver diseases [1]. HCV core protein-transgenic mice develop hepatic steatosis due to impaired β-oxidation caused by mitochondrial. In patients with impaired hepatic mitochondrial β-oxidation, ketogenesis is expected to be inadequate. Adult-onset type 2 citrullinemia (CTLN2) has been demonstrated to present as non-alcoholic fatty liver disease (NAFLD) [3]. CTLN 2 is associated with mutations in the SLC25A13 gene encoding citrin, which is a component of the mitochondrial malate-aspartate shuttle. Functional defectiveness of citrin impairs transport of aspartate from mitochondria but that of NADH into mitochondria
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