NDLI: Monascin improves diabetes and dyslipidemia by regulating PPARγ and inhibiting lipogenesis in fructose-rich diet-induced C57BL/6 mice

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Monascin improves diabetes and dyslipidemia by regulating PPARγ and inhibiting lipogenesis in fructose-rich diet-induced C57BL/6 mice

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Food & Function Vol - 4 Issue - 5

Food & Function Vol - 4 Issue - 4

Food & Function Vol - 4 Issue - 3

Food & Function Vol - 4 Issue - 2

Food & Function Vol -3

Food & Function Vol -2

Food & Function Vol -1

Monascin improves diabetes and dyslipidemia by regulating PPARγ and inhibiting lipogenesis in fructose-rich diet-induced C57BL/6 mice

Content Provider	Royal Society of Chemistry (RSC)
Author	Hsu, Wei-Hsuan Pan, Tzu-Ming Chang, Yu-Yin Hsu, Ya-Wen Lee, Bao-Hong Huang, Tao
Copyright Year	2013
Abstract	Monascin (MS) is a yellow compound isolated from Monascus-fermented products that has pancreatic protective, anti-inflammatory, anti-oxidative, and hypolipidemic activity. We recently found that MS also acts as a peroxisome proliferator-activated receptor-gamma (PPARγ) agonist, thereby promoting insulin sensitivity in C2C12 cells. However, the attenuation of hyperglycemia by MS treatment in vivo remains uncertain. In the present study, both MS and pioglitazone significantly down-regulated blood glucose and hyperinsulinemia in fructose-rich diet (FRD)-induced C57BL/6 mice (8 weeks). In addition, inhibitions of inflammatory factor production, serum dyslipidemia, and hepatic fatty acid accumulation by MS and pioglitazone were attenuated by GW9662 (PPARγ antagonist). These results were mediated by MS-suppressing FRD-elevated lipogenic transcription factors, including sterol regulatory element-binding protein-1c (SREBP-1c), carbohydrate response element-binding protein (ChREBP), PPARγ coactivator-1α (PGC-1α), and PPARγ coactivator-1β (PGC-1β). Taken together, de novo lipogenesis results in hyperlipidemia and hyperglycemia by fructose induction thereby leading to diabetes development; we found that MS may inhibit lipogenesis in FRD-induced mice. These findings suggest that MS acts as an antidiabetic agent and thus may have therapeutic potential for prevention of diabetes.
Starting Page	950
Ending Page	959
Page Count	10
File Format	HTM / HTML PDF
ISSN	20426496
Volume Number	4
Issue Number	6
Journal	Food & Function
DOI	10.1039/c3fo60062a
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Lipid-lowering agent Peroxisome Peroxisome proliferator-activated receptor gamma Agonist Insulin Hyperglycemia Pioglitazone Glucose Hyperinsulinemia Dyslipidemia Fatty acid Sterol regulatory element-binding protein Carbohydrate Protein Carbohydrate-responsive element-binding protein Transcription coregulator PPARGC1A Lipogenesis Hyperlipidemia Fructose Diabetes mellitus type 2 Anti-diabetic medication
Content Type	Text
Resource Type	Article
Subject	Medicine Food Science

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