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Background: RBE is known as nutritious bioactive compounds and is proven to decrease blood lipids, hepatic fat accumulation and oxidative damage. However, the molecular mechanisms of protective effect of RBE has not been clarified.
Objective: To investigate the effect and mechanism of RBE on hepatic lipid accumulation and lipid oxidative damage in rats fed a high-fat diet (HFD).
Material and Method: Male Sprague-Dawley rats were divided into four groups including 1) control group (C), 2) high-fat diet fed only group (HF), 3) HF co-fed with RBE at the dose of 2,205 mg/kg/day (HFR1 group) and 4) HF co-fed with RBE at the dose of 4,410 mg/kg/day (HFR2 group), respectively. After four weeks, body weight, metabolic and oxidative damage markers were assessed.
Results: Body weight, abdominal fat tissue weight, liver weight, and serum lipid levels were reduced in RBE-treated rats compared to HFD alone-fed rats. RBE-fed groups showed significantly lower levels of total-cholesterol, triglyceride and malondialdehyde in the liver tissue. RBE also inhibited hepatic 3-hydroxy-3 methylglutaryl coenzyme A reductase (HMGCR) activity, suppressed expression of hepatic sterol regulatory element binding protein-1 (SREBP-1) and nuclear factor kappa B (NF-kappa B), and up-regulated hepatic adenosine monophosphate-activated protein kinase (AMPK) expression.
Conclusion: RBE improves hepatic fat accumulation via the regulation of SREBP-1, AMPK expression and HMGCR activity in HFD induced obese rats. RBE also attenuates the damaging effects of oxidative stress by decreasing lipid peroxidation and NF-kappa B expression in the liver. Thus, RBE may be useful in the management of dyslipidemia and oxidative stress at the onset of obesity.
Keywords: Rice bran, Fat metabolism, Non-alcoholic fatty liver disease, Oxidative stress