Document Detail


Mangiferin decreases plasma free fatty acids through promoting its catabolism in liver by activation of AMPK.
MedLine Citation:
PMID:  22292039     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mangiferin has been shown to have the effect of improving dyslipidemia. Plasma free fatty acids (FFA) are closely associated with blood lipid metabolism as well as many diseases including metabolic syndrome. This study is to investigate whether mangiferin has effects on FFA metabolism in hyperlipidemic rats. Wistar rats were fed a high-fat diet and administered mangiferin simultaneously for 6 weeks. Mangiferin (50, 100, 150 mg/kg BW) decreased dose-dependently FFA and triglycerides (TG) levels in plasma, and their accumulations in liver, but increased the β-hydroxybutyrate levels in both plasma and liver of hyperlipidemic rats. HepG2 cells were treated with oleic acid (OA, 0.2 mmol/L) to simulate the condition of high level of plasma FFA in vitro, and were treated with different concentrations of mangiferin simultaneously for 24 h. We found that mangiferin significantly increased FFA uptake, significantly decreased intracellular FFA and TG accumulations in HepG2 cells. Mangiferin significantly increased AMP-activated protein kinase (AMPK) phosphorylation and its downstream proteins involved in fatty acid translocase (CD36) and carnitine palmitoyltransferase 1 (CPT1), but significantly decreased acyl-CoA: diacylgycerol acyltransferase 2 (DGAT2) expression and acetyl-CoA carboxylase (ACC) activity by increasing its phosphorylation level in both in vivo and in vitro studies. Furthermore, these effects were reversed by Compound C, an AMPK inhibitor in HepG2 cells. For upstream of AMPK, mangiferin increased AMP/ATP ratio, but had no effect on LKB1 phosphorylation. In conclusion, mangiferin decreased plasma FFA levels through promoting FFA uptake and oxidation, inhibiting FFA and TG accumulations by regulating the key enzymes expression in liver through AMPK pathway. Therefore, mangiferin is a possible beneficial natural compound for metabolic syndrome by improving FFA metabolism.
Authors:
Yucun Niu; Songtao Li; Lixin Na; Rennan Feng; Liyan Liu; Ying Li; Changhao Sun
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Publication Detail:
Type:  Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-01-23
Journal Detail:
Title:  PloS one     Volume:  7     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2012  
Date Detail:
Created Date:  2012-01-31     Completed Date:  2012-06-04     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e30782     Citation Subset:  IM    
Affiliation:
Department of Nutrition and Food Hygiene, Public Health College, Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Adenylate Kinase / metabolism*
Animals
Down-Regulation / drug effects
Enzyme Activation / drug effects
Fatty Acids, Nonesterified / blood*
Female
Hep G2 Cells
Humans
Hyperlipidemias / blood,  metabolism
Hypoglycemic Agents / pharmacology
Lipid Metabolism / drug effects
Liver / drug effects*,  metabolism
Male
Metabolism / drug effects
Rats
Rats, Wistar
Triglycerides / blood,  metabolism
Xanthones / pharmacology*
Chemical
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 0/Hypoglycemic Agents; 0/Triglycerides; 0/Xanthones; 1M84LD0UMD/mangiferin; EC 2.7.4.3/Adenylate Kinase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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