Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 9 (1), 27

Black Rice (Oryza Sativa L.) Extract Attenuates Hepatic Steatosis in C57BL/6 J Mice Fed a High-Fat Diet via Fatty Acid Oxidation

Affiliations

Black Rice (Oryza Sativa L.) Extract Attenuates Hepatic Steatosis in C57BL/6 J Mice Fed a High-Fat Diet via Fatty Acid Oxidation

Hwan-Hee Jang et al. Nutr Metab (Lond).

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)-α (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 β-oxidation and ω-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.

Figures

Figure 1
Figure 1
Liquid chromatograms of anthocyanin extracted from BRE (A), C3G standard (B), and P3G standard (C). Peak 1, Cyanidin 3,5-diglucoside; Peak 2, Cyanidin-3-glucoside; Peak 3, peonidin-3-glucoside; Peak 4, unknown (cyanidin-based).
Figure 2
Figure 2
Effect of BRE supplementation on serum lipid concentration. Concentrations of serum FFAs (A), TG (B), TC (C), HDL- C (D), LDL-C (E), and HDL/LDL-C ratio (F) for each group during 7-wk feeding experiments. Data are expressed as mean ± standard error (n = 8 per group). Means with different letters (a, b, or c) on the bar are significantly different from each other at p < 0.05 by Duncan's multiple range test.
Figure 3
Figure 3
Effect of BRE supplementation on blood concentration of glucose and insulin. Concentrations of fasting blood glucose (A), and serum insulin (B), and insulin resistance index (C) for each group during 7-wk feeding experiments. HOMA-IR = fasting glucose (mg/dl) × fasting insulin (mU/L)/405. Data are expressed as mean ± standard error (n = 8 per group). Means with different letters (a, b, or c) on the bar are significantly different from each other at p < 0.05 by Duncan's multiple range test.
Figure 4
Figure 4
Effect of BRE supplementation on liver histology. Photomicrographs of H&E stained longitudinal liver sections from representative animals in the ND, HF, and HF + BRE1% groups (magnification 400×) (A). Lipid droplets (arrows), microvesicular steatosis (arrow head), and mild inflammation (circle) were observed in the HF liver sections. The HF group had a higher mean hepatic steatosis grade (0-3 scale) than the ND and HF + BRE1% groups (B). Data are expressed as means ± standard error (n = 8 per group). Means with different letters (a, b, or c) on their associated bars are significantly different from each other at p < 0.05 by Duncan's multiple range test.
Figure 5
Figure 5
Effect of BRE supplementation on mRNA levels of PPAR-α (A), CPT1A (B), ACO (C), and CYP4A10 (D) in liver of mice that were fed different diets. Data are expressed as mean ± standard error (n = 8 per group). Means with different letters (a, b, or c) on the bar are significantly different from each other at p < 0.05 by Duncan's multiple range test.

Similar articles

See all similar articles

Cited by 17 articles

See all "Cited by" articles

References

    1. Yeon JE, Choi KM, Baik SH, Kim KO, Lim HJ, Park KH, Kim JY, Park JJ, Kim JS, Bak YT, Byun KS, Lee CH. Reduced expression of peroxisome proliferator-activated receptor-alpha may have an important role in the development of non-alcoholic fatty liver disease. J Gastroenterol Hepatol. 2004;19:799–804. doi: 10.1111/j.1440-1746.2004.03349.x. - DOI - PubMed
    1. Ji G, Zhao X, Leng L, Liu P, Jiang Z. Comparison of dietary control and atorvastatin on high fat diet induced hepatic steatosis and hyperlipidemia in rats. Lipids Health Dis. 2011;10:23. doi: 10.1186/1476-511X-10-23. - DOI - PMC - PubMed
    1. Samuel VT, Liu ZX, Wang A, Beddow SA, Geisler JG, Kahn M, Zhang XM, Monia BP, Bhanot S, Shulman GI. Inhibition of protein kinase cepsilon prevents hepatic insulin resistance in nonalcoholic fatty liver disease. J Clin Invest. 2007;117:739–745. doi: 10.1172/JCI30400. - DOI - PMC - PubMed
    1. Samuel VT, Liu ZX, Qu X, Elder BD, Bilz S, Befroy D, Romanelli AJ, Shulman GI. Mechanism of hepatic insulin resistance in non-alcoholic fatty liver disease. J Biol Chem. 2004;279:32345–32353. doi: 10.1074/jbc.M313478200. - DOI - PubMed
    1. Musso G, Gambino R, Cassader M. Recent insights into hepatic lipid metabolism in non-alcoholic fatty liver disease (NAFLD) Prog Lipid Res. 2009;48:1–26. doi: 10.1016/j.plipres.2008.08.001. - DOI - PubMed

LinkOut - more resources

Feedback