期刊
JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION
卷 54, 期 3, 页码 190-197出版社
JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION
DOI: 10.3164/jcbn.13-74
关键词
non-alcoholic fatty liver disease; alpha-tocopherol; alpha-tocopherol transfer protein; antioxidant
资金
- Japan Society for the Promotion of Science [17591122, 23591589]
- Mitsui Life Social Welfare Foundation
- Kao Research Council for the Study of Healthcare Science
- Osaka Medical Research Foundation for Incurable Disease
- Grants-in-Aid for Scientific Research [23591589, 17591122] Funding Source: KAKEN
Non-alcoholic fatty liver disease is the most common liver disorder in developed countries, and its incidence is increasing in all population groups. As an antioxidant, vitamin E is effective in the treatment of non-alcoholic fatty liver disease, although the mechanism is still unclear. Methionine-choline deficient Wistar rats (n = 5) used as an experimental model of non-alcoholic fatty liver disease were fed a vitamin E-enriched diet (500 mg/kg) for 4 weeks. The effects were assessed by measuring lipid peroxidation, alpha-tocopherol levels, and the expression of alpha-tocopherol-related proteins in the liver. In vitamin E-treated methionine-choline deficient rats, lipid peroxidation was reduced, but liver histopathological changes were not improved. Hepatic alpha-tocopherol levels in these rats were significantly elevated compared to normal rats treated with vitamin E. Expression of liver alpha-tocopherol transfer protein in vitamin E-treated methionine-choline deficient rats was significantly repressed compared to methionine-choline deficient rats. The expression of liver cytochrome P450 4F2 and ATP-binding cassette transporter protein 1, involved in metabolism and transport of alpha-tocopherol, respectively, was significantly repressed in vitamin E-treated methionine-choline deficient rats. In methionine-choline deficient rats, vitamin E treatment altered the hepatic alpha-tocopherol-related protein expression, which may affect alpha-tocopherol status in the liver, leading to reduced lipid peroxidation.
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