Document Detail


Free fatty acids link metabolism and regulation of the insulin-sensitizing fibroblast growth factor-21.
MedLine Citation:
PMID:  19401423     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Fibroblast growth factor (FGF)-21 improves insulin sensitivity and lipid metabolism in obese or diabetic animal models, while human studies revealed increased FGF-21 levels in obesity and type 2 diabetes. Given that FGF-21 has been suggested to be a peroxisome proliferator-activator receptor (PPAR) alpha-dependent regulator of fasting metabolism, we hypothesized that free fatty acids (FFAs), natural agonists of PPARalpha, might modify FGF-21 levels. RESEARCH DESIGN AND METHODS: The effect of fatty acids on FGF-21 was investigated in vitro in HepG2 cells. Within a randomized controlled trial, the effects of elevated FFAs were studied in 21 healthy subjects (13 women and 8 men). Within a clinical trial including 17 individuals, the effect of insulin was analyzed using an hyperinsulinemic-euglycemic clamp and the effect of PPARgamma activation was studied subsequently in a rosiglitazone treatment trial over 8 weeks. RESULTS: Oleate and linoleate increased FGF-21 expression and secretion in a PPARalpha-dependent fashion, as demonstrated by small-interfering RNA-induced PPARalpha knockdown, while palmitate had no effect. In vivo, lipid infusion induced an increase of circulating FGF-21 in humans, and a strong correlation between the change in FGF-21 levels and the change in FFAs was observed. An artificial hyperinsulinemia, which was induced to delineate the potential interaction between elevated FFAs and hyperinsulinemia, revealed that hyperinsulinemia also increased FGF-21 levels in vivo, while rosiglitazone treatment had no effect. CONCLUSIONS: The results presented here offer a mechanism explaining the induction of the metabolic regulator FGF-21 in the fasting situation but also in type 2 diabetes and obesity.
Authors:
Knut Mai; Janin Andres; Katrin Biedasek; Jessica Weicht; Thomas Bobbert; Markus Sabath; Sabine Meinus; Franziska Reinecke; Matthias Möhlig; Martin O Weickert; Markus Clemenz; Andreas F H Pfeiffer; Ulrich Kintscher; Simone Spuler; Joachim Spranger
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-04-28
Journal Detail:
Title:  Diabetes     Volume:  58     ISSN:  1939-327X     ISO Abbreviation:  Diabetes     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-30     Completed Date:  2009-07-29     Revised Date:  2010-09-27    
Medline Journal Info:
Nlm Unique ID:  0372763     Medline TA:  Diabetes     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1532-8     Citation Subset:  AIM; IM    
Affiliation:
Department of Endocrinology, Diabetes and Nutrition, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
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MeSH Terms
Descriptor/Qualifier:
Cell Line
Diabetes Mellitus, Type 2 / complications,  drug therapy,  metabolism*
Fasting / physiology*
Fatty Acids, Nonesterified / metabolism*
Female
Fibroblast Growth Factors / genetics,  metabolism*
Gene Expression Regulation / drug effects
Glucose Clamp Technique
Glycerol / pharmacology
Homeostasis
Humans
Hyperinsulinism / metabolism,  physiopathology
Hypoglycemic Agents / therapeutic use
Lecithins / pharmacology
Male
Obesity / complications,  metabolism
PPAR alpha / genetics,  physiology
PPAR gamma / genetics,  physiology*
RNA, Messenger / genetics
Reference Values
Thiazolidinediones / therapeutic use*
Chemical
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 0/Hypoglycemic Agents; 0/Lecithins; 0/PPAR alpha; 0/PPAR gamma; 0/RNA, Messenger; 0/Thiazolidinediones; 0/fibroblast growth factor 21; 122320-73-4/rosiglitazone; 56-81-5/Glycerol; 62031-54-3/Fibroblast Growth Factors
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