Format

Send to

Choose Destination
J Agric Food Chem. 2010 Dec 22;58(24):12703-9. doi: 10.1021/jf103121c. Epub 2010 Nov 16.

The effect of Monascus secondary polyketide metabolites, monascin and ankaflavin, on adipogenesis and lipolysis activity in 3T3-L1.

Author information

1
Department of Biochemical Science & Technology, College of Life Science, National Taiwan University, Taipei, Taiwan.

Abstract

The aim of the present work is to investigate the effects of Monascus secondary metabolites, monascin (MS) and ankaflavin (AK), on cell proliferation, adipogenesis, lipolysis and heparin-releasable lipoprotein lipase (HR-LPL) in 3T3-L1 preadipocyte. MS and AK inhibit the proliferation of 3T3-L1 cells in a dose-dependent fashion. At 8 μg/mL concentration MS inhibits proliferation for 80.5% after 48 h, whereas the value for AK is 69.2%. Adipogenesis is inhibited by MS and AK without dose-dependency. Triglyceride is decreased 37.1% and 41.1% respectively by treating 0.125 μg/mL MS and AK. Adipocyte-specific transcription factors peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein β (C/EBPβ), C/EBPδ and C/EBPα mRNA levels are measured by real-time polymerase chain reaction. The expression of the four transcriptional factors analyzed (PPARγ, C/EBPβ, C/EBPδ and C/EBPα) is reduced at the initial and the middle period. At the later period, there is no effect on the expression of PPARγ and C/EBPα by treating MS and AK. Furthermore, both MS and AK increase basal lipolysis of mature adipocytes by 113.2% and 278.3% upregulation, respectively. And both MS and AK reduce the activity of HR-LPL, by 45.3% and 58.1% reduction, respectively. This study reveals for the first time that Monascus secondary metabolites, MS and AK, can prevent the differentiation of preadipocyte and stimulate basal lipolysis of mature adipocytes, avoiding the accumulation of lipid.

PMID:
21080714
DOI:
10.1021/jf103121c
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for American Chemical Society
Loading ...
Support Center