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Black rice (Oryza sativa L.) extract attenuates hepatic steatosis in C57BL/6 J mice fed a high-fat diet via fatty acid oxidation

Cited 70 time in Web of Science Cited 95 time in Scopus
Authors

Jang, Hwan-Hee; Park, Mi-Young; Kim, Heon-Woong; Lee, Young-Min; Hwang, Kyung-A; Park, Jae-Hak; Park, Dong-Sik; Kwon, Oran

Issue Date
2012-04
Publisher
BioMed Central
Citation
Nutrition and Metabolism, Vol.9, p. 27
Abstract
Background: Two major risk factors for the onset of fatty liver disease are excessive alcohol intake and obesity, the latter being associated with non-alcoholic fatty liver disease (NAFLD). The aim of this study was to examine the effects of black rice extract (BRE) on hepatic steatosis and insulin resistance in high-fat diet-fed mice, providing a model of NAFLD. Methods: Twenty-four mice were randomly divided into three groups (n = 8 in each group): normal fat diet (ND), high fat diet (HF), and high fat diet supplemented with 1% (w/w) BRE (HF + 1% BRE). The experimental diets were fed for seven weeks. Results: A HF induced hepatic steatosis with significant increases in the serum levels of free fatty acids (FFAs), triglyceride (TG), total cholesterol (TC), and insulin. By contrast, supplementary BRE (10 g/kg of diet) included in the HF alleviated hepatic steatosis and significantly decreased serum TG and TC levels (p < 0.01 for both). Dietary BRE also increased expression of fatty acid metabolism-related genes, including carnitine palmitoyltransferase (CPT1A), acyl-CoA oxidase (ACO), cytochrome P450 (CYP4A10), and peroxisome proliferator activated receptor (PPAR)-alpha (p < 0.05 for all). Conclusions: Dietary BRE supplementation improved serum lipid profiles and significantly enhanced mRNA expression levels of fatty acid metabolism-related genes, primarily via beta-oxidation and omega-oxidation in the liver. Taken together, these findings suggest that a BRE-supplemented diet could be useful in reducing the risks of hepatic steatosis and related disorders, including hyperlipidemia and hyperglycemia.
ISSN
1743-7075
URI
https://hdl.handle.net/10371/194806
DOI
https://doi.org/10.1186/1743-7075-9-27
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  • College of Veterinary Medicine
  • Department of Veterinary Medicine
Research Area Laboratory Animal Medicine, Toxicologic Pathology

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