To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Adipocyte-specific overex… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

Adipocyte-specific overexpression of FOXC2 prevents diet-induced increases in intramuscular fatty acyl CoA and insulin resistance.

Journal article
Authors Jason K Kim
Hyo-Jeong Kim
So-Young Park
Anna Cederberg
Rickard Westergren
Daniel Nilsson
Takamasa Higashimori
You-Ree Cho
Zhen-Xiang Liu
Jianying Dong
Gary W Cline
Sven Enerbäck
Gerald I Shulman
Published in Diabetes
Volume 54
Issue 6
Pages 1657-63
ISSN 0012-1797
Publication year 2005
Published at Institute of Medical Biochemistry
Pages 1657-63
Language en
Keywords Acyl Coenzyme A, metabolism, Adipocytes, metabolism, Animals, DNA-Binding Proteins, biosynthesis, genetics, physiology, Dietary Fats, metabolism, Forkhead Transcription Factors, Gene Expression, Insulin, metabolism, Insulin Resistance, Male, Mice, Mice, Transgenic, Muscle, Skeletal, metabolism, Signal Transduction, Transcription Factors, biosynthesis, genetics, physiology
Subject categories Medical and Health Sciences


Insulin resistance plays a major role in the development of type 2 diabetes and may be causally associated with increased intracellular fat content. Transgenic mice with adipocyte-specific overexpression of FOXC2 (forkhead transcription factor) have been generated and shown to be protected against diet-induced obesity and glucose intolerance. To understand the underlying mechanism, we examined the effects of chronic high-fat feeding on tissue-specific insulin action and glucose metabolism in the FOXC2 transgenic (Tg) mice. Whole-body fat mass were significantly reduced in the FOXC2 Tg mice fed normal diet or high-fat diet compared with the wild-type mice. Diet-induced insulin resistance in skeletal muscle of the wild-type mice was associated with defects in insulin signaling and significant increases in intramuscular fatty acyl CoA levels. In contrast, FOXC2 Tg mice were completely protected from diet-induced insulin resistance and intramuscular accumulation of fatty acyl CoA. High-fat feeding also blunted insulin-mediated suppression of hepatic glucose production in the wild-type mice, whereas FOXC2 Tg mice were protected from diet-induced hepatic insulin resistance. These findings demonstrate an important role of adipocyte-expressed FOXC2 on whole-body glucose metabolism and further suggest FOXC2 as a novel therapeutic target for the treatment of insulin resistance and type 2 diabetes.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?