Fenofibrate, a peroxisome proliferator‐activated receptor α agonist, reduces hepatic steatosis and lipid peroxidation in fatty liver Shionogi mice with hereditary fatty …
Y Harano, K Yasui, T Toyama, T Nakajima… - Liver …, 2006 - Wiley Online Library
Y Harano, K Yasui, T Toyama, T Nakajima, H Mitsuyoshi, M Mimani, T Hirasawa, Y Itoh…
Liver International, 2006•Wiley Online LibraryBackground and aims: The fatty liver Shionogi (FLS) mouse, a unique model for
nonalcoholic fatty liver disease (NAFLD), is an inbred strain that develops spontaneous
hepatic steatosis without obesity or diabetes mellitus. Peroxisome proliferator‐activated
receptor (PPAR) α controls fatty acid metabolism. In the present study, we investigated the
effect of fenofibrate, a PPARα agonist, on hepatic steatosis in FLS mice. Methods: Thirteen‐
week‐old FLS mice were fed a diet with 0.1% fenofibrate (w/w) for 12 days. The degree of …
nonalcoholic fatty liver disease (NAFLD), is an inbred strain that develops spontaneous
hepatic steatosis without obesity or diabetes mellitus. Peroxisome proliferator‐activated
receptor (PPAR) α controls fatty acid metabolism. In the present study, we investigated the
effect of fenofibrate, a PPARα agonist, on hepatic steatosis in FLS mice. Methods: Thirteen‐
week‐old FLS mice were fed a diet with 0.1% fenofibrate (w/w) for 12 days. The degree of …
Abstract: Background and aims: The fatty liver Shionogi (FLS) mouse, a unique model for nonalcoholic fatty liver disease (NAFLD), is an inbred strain that develops spontaneous hepatic steatosis without obesity or diabetes mellitus. Peroxisome proliferator‐activated receptor (PPAR) α controls fatty acid metabolism. In the present study, we investigated the effect of fenofibrate, a PPARα agonist, on hepatic steatosis in FLS mice.
Methods: Thirteen‐week‐old FLS mice were fed a diet with 0.1% fenofibrate (w/w) for 12 days. The degree of hepatic steatosis was estimated by histological examination and hepatic triglyceride levels. Expression levels of genes involved in fatty acid turnover, including Acox1, Cpt1a, Fabp1, Acadl, and Acadm, were determined by Northern blot analyses. We measured levels of lipid peroxidation, glutathione, and anti‐oxidative enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, in the liver.
Result: Treatment of FLS mice with fenofibrate improved hepatic steatosis by activating expression of genes involved in fatty acid turnover and decreased hepatic lipid peroxidation. Fenofibrate increased the activity of catalase by upregulating its mRNA levels.
Conclusion: Fenofibrate, which is currently used in therapy of hyperlipidemia, might also be useful for treating patients with NAFLD even in cases where NAFLD is not associated with obesity or diabetes mellitus.
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