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Steatosis and hepatic expression of genes regulating lipid metabolism in Japanese patients infected with hepatitis C virus

  • Original Article—Liver, Pancreas, and Biliary Tract
  • Published:
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Abstract

Purpose

Steatosis is a histological finding associated with the progression of chronic hepatitis C. The aims of this study were to elucidate risk factors associated with steatosis and to evaluate the association between steatosis and hepatic expression of genes regulating lipid metabolism.

Methods

We analyzed 297 Japanese patients infected with hepatitis C virus and a subgroup of 100 patients who lack metabolic factors for steatosis. We determined intrahepatic mRNA levels of 18 genes regulating lipid metabolism in these 100 patients using real-time reverse transcription-polymerase chain reaction. Levels of peroxisome proliferator-activated receptor α and sterol regulatory element-binding protein 1 proteins were assessed by immunohistochemistry.

Results

Steatosis was present in 171 (57%) of 297 patients. The presence of steatosis was independently associated with a higher body mass index, higher levels of γ-glutamyl transpeptidase and triglyceride, and a higher fibrosis stage. Steatosis was present in 43 (43%) of 100 patients lacking metabolic factors. Levels of mRNA and protein of peroxisome proliferator-activated receptor α, which regulates β-oxidation of fatty acid, were lower in patients with steatosis than in patients without steatosis.

Conclusions

These findings indicate that impaired degradation of lipid may contribute to the development of hepatitis C virus-related steatosis.

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Acknowledgments

This work was supported by a Grant-in-Aid for Scientific Research from the Japan Society for the Program of Science (20590408) and by a grant from Ministry of Health, Labor and Welfare of Japan (H20-hepatitis-008; to K. Yasui).

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Correspondence to Kohichiroh Yasui.

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Yasui, K., Harano, Y., Mitsuyoshi, H. et al. Steatosis and hepatic expression of genes regulating lipid metabolism in Japanese patients infected with hepatitis C virus. J Gastroenterol 45, 95–104 (2010). https://doi.org/10.1007/s00535-009-0133-8

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  • DOI: https://doi.org/10.1007/s00535-009-0133-8

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