Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice

Nov 27, 2013Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

Natural compounds Monascin and Ankaflavin may reduce fatty liver disease by activating energy and fat metabolism pathways in high-fat diet mice

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Abstract

Monascin (MS) and ankaflavin (AK) significantly attenuated high-fat diet-induced elevation of total cholesterol and triglycerides in mice.

MS and AK are secondary metabolites from Monascus-fermented products with potential effects on nonalcoholic fatty liver disease (NAFLD).
Both compounds prevented fatty acid accumulation in liver cells by inhibiting the uptake of fatty acids and promoting their breakdown.
MS and AK activated specific receptors and enzymes (PPAR-α and AMPK) that are involved in fatty acid metabolism.
The administration of MS and AK resulted in a reduction of several lipids in the plasma, including total cholesterol and low-density lipoprotein cholesterol.
MS and AK may modulate gene expression related to liver fat accumulation and inflammation.

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Yellow pigments monascin (MS) and ankaflavin (AK) are secondary metabolites derived from Monascus-fermented products. The hypolipidemic and anti-inflammatory effects of MS and AK indicate that they have potential on preventing or curing nonalcoholic fatty liver disease (NAFLD). Oleic acid (OA) and high-fat diet were used to induce steatosis in FL83B hepatocytes and NAFLD in mice, respectively. We found that both MS and AK prevented fatty acid accumulation in hepatocytes by inhibiting fatty acid uptake, lipogenesis, and promoting fatty acid beta-oxidation mediated by activating peroxisome proliferator-activated receptor (PPAR)-α and AMP-activated kinase (AMPK). Furthermore, MS and AK significantly attenuated high-fat diet-induced elevation of total cholesterol (TC), triaceylglycerol (TG), free fatty acid (FFA), and low density lipoprotein-cholesterol (LDL-C) in plasma. MS and AK promoted AMPK phosphorylation, suppressed the steatosis-related mRNA expression and inflammatory cytokines secretion, as well as upregulated farnesoid X receptor (FXR), peroxisome proliferator-activated receptor gamma co-activator (PGC)-1α, and PPARα expression to induce fatty acid oxidation in the liver of mice. We provided evidence that MS and AK act as PPARα agonists to upregulate AMPK activity and attenuate NAFLD. MS and AK may be supplied in food supplements or developed as functional foods to reduce the risk of diabetes and obesity.

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Monascin and ankaflavin act as natural AMPK activators with PPARα agonist activity to down-regulate nonalcoholic steatohepatitis in high-fat diet-fed C57BL/6 mice

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