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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.
Food Chem Toxicol 2014; 64:94-103FC

Abstract

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.

Authors+Show Affiliations

Department of Biochemical Science & Technology, College of Life Science, National Taiwan University, No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan.Department of Biochemical Science & Technology, College of Life Science, National Taiwan University, No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan.Department of Biochemical Science & Technology, College of Life Science, National Taiwan University, No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan.R&D Division, SunWay Biotechnology Company Limited, Taipei, Taiwan.Department of Biochemical Science & Technology, College of Life Science, National Taiwan University, No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan. Electronic address: tmpan@ntu.edu.tw.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

24275089

Citation

Hsu, Wei-Hsuan, et al. "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." Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, vol. 64, 2014, pp. 94-103.
Hsu WH, Chen TH, Lee BH, et al. 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. Food Chem Toxicol. 2014;64:94-103.
Hsu, W. H., Chen, T. H., Lee, B. H., Hsu, Y. W., & Pan, T. M. (2014). 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. Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, 64, pp. 94-103. doi:10.1016/j.fct.2013.11.015.
Hsu WH, et al. 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. Food Chem Toxicol. 2014;64:94-103. PubMed PMID: 24275089.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Hsu,Wei-Hsuan, AU - Chen,Ting-Hung, AU - Lee,Bao-Hong, AU - Hsu,Ya-Wen, AU - Pan,Tzu-Ming, Y1 - 2013/11/22/ PY - 2013/03/05/received PY - 2013/09/18/revised PY - 2013/11/13/accepted PY - 2013/11/27/entrez PY - 2013/11/28/pubmed PY - 2014/9/23/medline KW - ACC KW - ACOX KW - ACS KW - AK KW - ALT KW - AMP-activated kinase KW - AMPK KW - AST KW - Ankaflavin (AK) KW - BSA KW - CPT-1 KW - CV KW - DMSO KW - ELISA KW - FABP KW - FAS KW - FAT KW - FBS KW - FFA KW - FXR KW - GLUT KW - H&E KW - HAECs KW - HDL-C KW - HPLC KW - HUVECs KW - IACUC KW - ICAM-1 KW - IL-6 KW - Institutional Animal Care and Use Committee KW - JNK KW - LDL-C KW - MS KW - MTP KW - Monascin (MS) KW - NAFLD KW - NASH KW - NCBI KW - NF-κB KW - National Center for Biotechnology Information KW - Nonalcoholic fatty liver disease (NAFLD) KW - Nrf2 KW - OA KW - Oleic acid (OA) KW - PCR KW - PGC-1α KW - PPARα KW - PPARγ KW - PPREs KW - PTP1B KW - Peroxisome proliferator-activated receptor (PPAR)-α KW - SDS KW - SPPARMs KW - SREBP-1c KW - TC KW - TG KW - TGFβ KW - TLC KW - TNF-α KW - TR-FRET KW - TZDs KW - Tyr KW - VCAM-1 KW - acetyl-CoA carboxylase KW - acyl-CoA oxidase KW - acyl-CoA synthetase KW - alanine aminotranferase KW - ankaflavin KW - aspartate transaminase KW - bovine serum albumin KW - c-Jun NH(2)-terminal kinase KW - cardiovascular KW - carnitine palmitoyl transferase I KW - dimethyl sulfoxide KW - enzyme-linked immunosorbent assay KW - farnesoid X receptor KW - fatty acid synthase KW - fatty acid transporter KW - fatty acid-binding protein KW - fetal bovine serum KW - free fatty acid KW - glucose transporter KW - hematoxylin and eosin KW - high-density lipoprotein cholesterol KW - high-performance liquid chromatography KW - human aortic endothelial cells KW - human umbilical vein endothelial cells KW - iNOS KW - inducible nitric oxide synthase KW - intercellular adhesion molecule-1 KW - interleukin-6 KW - low density lipoprotein-cholesterol KW - microsomal triglyceride transfer protein KW - monascin KW - nonalcoholic fatty liver disease KW - nonalcoholic steatohepatitis KW - nuclear factor erythroid 2-related factor 2 KW - nuclear factor-kappaB KW - oleic acid KW - peroxisome proliferator activated receptor alpha KW - peroxisome proliferator activated receptor gamma KW - peroxisome proliferator-activated receptor gamma co-activator 1-alpha KW - peroxisome-proliferator-response elements KW - polymerase chain reaction KW - protein tyrosine phosphatase 1B KW - selective PPAR modulators KW - sodium dodecyl sulfate KW - sterol regulatory element-binding protein KW - thiazolidinediones KW - thin layer chromatography KW - time-resolved fluorescence resonance energy transfer KW - total cholesterol KW - transformation growth factor beta KW - triaceylglycerol KW - tumor necrosis factor-alpha KW - tyrosine KW - vascular cell adhesion molecule-1 SP - 94 EP - 103 JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association JO - Food Chem. Toxicol. VL - 64 N2 - 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. SN - 1873-6351 UR - https://www.unboundmedicine.com/medline/citation/24275089/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_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0278-6915(13)00774-6 DB - PRIME DP - Unbound Medicine ER -