Pre-germinated brown rice alleviates non-alcoholic fatty liver disease induced by high fructose and high fat intake in rat

Abstract

In past researches, we had been proved the action mechanism of pre-germinated brown rice (PGBR) to treat metabolic syndrome and diabetes mellitus. This study was to investigate the protective effect of PGBR in high fructose and high fat-induced non-alcoholic fatty liver disease (NAFLD) in rodents. WKY rats were divided into: Control group was fed normal drinking water and diet; FLD group was fed 10% high-fructose-water (HFW) and high-fat-diet (HFD); PGBR group was given HFW, and HFD mixed PGBR. After four weeks, the body, hepatic and cardiac weight gains of FLD group had significant increases than that of Control group. The enhanced blood pressure and heart rate, hypertriglyceridemia, hyperuricemia, and higher liver function index (GPT levels) were observed; meanwhile, the IL-6 and TNF-α levels of serum, and TG level of liver were also elevated in FLD group. The related protein expressions of lipid synthesis, inflammation, cardiac fibrosis, and hypertrophy were deteriorated by HFW/HFD. However, in treatment group, PGBR decreased all above influenced parameters, additionally GOT; and related protein expressions. PGBR treated HFW/HFD-induced NAFLD and cardiac complications might be via improving lipid homeostasis, and inhibiting inflammation. Together, PGBR could be used as a healthy food for controlling NAFLD and its' cardiac dysfunction.

Keywords: NAFLD; PGBR; cardiac fibrosis and hypertrophy; inflammation.

Fig. 1.

The effects of PGBR on the fructose metabolism and lipid synthesis pathway in liver from NAFLD WKY. (A) Representative western blot images of protein bands. (B) Analysis of protein band density ratios after normalization against β-actin. Values are represented as means ± SD (n = 8). *p<0.05 (compared to Control group), ‍^#p<0.05 (compared to FLD group).

Fig. 2.

The effects of PGBR on the inflammatory signaling and antioxidant enzymes in liver from NAFLD WKY. (A) Representative western blot images of protein bands. (B) Analysis of protein band density ratios after normalization against β-actin. Values are represented as means ± SD (n = 8). *p<0.05 (compared to Control group), ‍^#p<0.05 (compared to FLD group).

Fig. 3.

The effects of PGBR on the inflammatory signaling in heart from NAFLD WKY. (A) Representative western blot images of protein bands. (B) Analysis of protein band density ratios after normalization against β-actin. Values are represented as means ± SD. (n = 8). *p<0.05 (compared to Control group), ‍^#p<0.05 (compared to FLD group).

Fig. 4.

The effects of PGBR on aberrant cardiac hypertrophy and fibrosis markers in heart from NAFLD WKY. (A) Representative western blot images of protein bands. (B) Analysis of protein bands density ratio after normalization against β-actin. Values are represented as means ± SD (n = 8). *p<0.05 (compared to control group), ‍^#p<0.05 (compared to DM group).

Fig. 5.

Hypothetical mechanisms of PGBR in high fructose/high fat intake-induced non-alcoholic fatty liver disease (NAFLD). The action mechanisms of PGBR ameliorating the metabolism of fructose and the biosynthesis of lipids, expression of PPARs and inflammation. Taken together, PGBR was able to ameliorate hypertriglyceridemia, hyperuricemia, liver function index, hepatic weight gain; and improved blood pressure and heart rate enhancement, cardiac hypertrophy and fibrosis, cardiac weight gain.