Abstract

The fermentation of brown rice produces black vinegar that has been suggested with beneficial metabolic effects; however, the mechanisms of actions of fermented brown rice have not been studied. We found that fermented brown rice extracts, especially a fraction of fermented brown rice fibers (FBRF), exhibited hypolipidemic and hypoglycemic activities in vivo. The oral administration of FBRF to C57BL/6J mice reduced plasma cholesterol, triglycerides, lowdensity- lipoprotein cholesterol levels, hepatic lipid accumulation and adipocyte size. The activation and induction of hepatic PPARα and subsequent regulation of its target gene expressions in fatty acid uptake and oxidation were the major mechanism for reducing plasma and hepatic triglyceride concentrations. In addition, FBRF improved glucose tolerance and insulin sensitivity. FBRF feeding reduced the expressions of hepatic ChREBP, a key transcription factor in gluconeogenesis, and pro-inflammatory cytokines, thus improved insulin resistance. These results demonstrated that FBR, especially FBRF, shows potent hypolipidemic and anti-diabetic activities through regulating the expression of genes associated with lipid, glucose metabolism and inflammatory cytokines.

Highlights

  • The mechanism of dyslipidemia causing cardiovascular disease (CVD) has been intensively investigated at the molecular level, providing evidence that an elevated level of low-density-lipoprotein (LDL) cholesterol is the major cause for CVD

  • This study investigates the role of fermented brown rice (FBR) and its fiber (FBRF) and small peptide fraction (FBRP) in regulating lipid and glucose metabolism, and suggests their potential application in the food industry

  • IL-6 a addition, the expression levels of phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6-phosphatase (G6Pase), which are essential enzymes in gluconeogenesis, were significantly decreased in the fermented brown rice fibers (FBRF), FBRP, and FBR groups (Figure 5A). These results indicated that the intake of FBRs improved glucose tolerance via downregulation of hepatic carbohydrateresponsive element binding proteins (ChREBP) expression and subsequent inhibited gluconeogenesis via reducing expression of PEPCK and G6Pase (Figure 6)

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Summary

Introduction

The mechanism of dyslipidemia causing cardiovascular disease (CVD) has been intensively investigated at the molecular level, providing evidence that an elevated level of low-density-lipoprotein (LDL) cholesterol is the major cause for CVD. Reducing LDL cholesterol has been a critical strategy in preventing CVD. In this regard, the efficacy study of a cholesterol-lowering treatment showed that an approximately 12% reduction in cholesterol leads to a reduction in the risk of CVD by 19% [1], and this level of reduction could be achieved through appropriate diet interventions. Several hypolipidemic drugs, including statins, are available; potent drugs usually have severe adverse effects. Statins could cause myopathy, peripheral neuropathy, and hepatotoxicity [2]. A great deal of effort has focused on the investigation of the biological function of natural compounds that could be applied to the prevention of CVD by dyslipidemia

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