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Am J Physiol Endocrinol Metab 291: E1092-E1099, 2006. First published July 5, 2006; doi:10.1152/ajpendo.00583.2005
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Differential regulation of intestinal lipid metabolism-related genes in obesity-resistant A/J vs. obesity-prone C57BL/6J mice

Hidehiko Kondo,1 Yoshihiko Minegishi,1 Yumiko Komine,1 Takuya Mori,1 Ichiro Matsumoto,2 Keiko Abe,2 Ichiro Tokimitsu,1 Tadashi Hase,1 and Takatoshi Murase1

1Biological Science Laboratories, Kao Corporation, Tochigi, Japan; and 2Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Science, The University of Tokyo, Tokyo, Japan

Submitted 28 November 2005 ; accepted in final form 28 June 2006

The effects of high-fat (HF) feeding on gene expression in the small intestine were examined using obesity-resistant A/J mice and obesity-prone C57BL/6J (B6) mice. Both strains of mice were maintained on low-fat (LF; 5% fat) or HF (30% fat) diets for 2 wk. Quantitative reverse transcription-PCR analysis revealed that lipid metabolism-related genes, including carnitine palmitoyltransferase (CPT) I, liver fatty acid binding protein, pyruvate dehydrogenase kinase-4, and NADP+-dependent cytosolic malic enzyme, were upregulated by HF feeding in both strains of mice. The upregulated gene expression levels were higher in A/J mice than in B6 mice, suggesting more active lipid metabolism in the small intestine of A/J mice. The prominent upregulation of the lipid metabolism-related genes were specific to the small intestine; the expression levels were little or unchanged in the liver, muscle, and white adipose tissue. The increase by HF feeding and predominant expression of the intestinal lipid metabolism-related genes in A/J mice were reflected in the enzyme activities; malic enzyme, CPT, and beta-oxidation activities were increased by HF feeding, and the upregulated malic enzyme and CPT activities were significantly higher in obesity-resistant A/J mice compared with those in obesity-prone B6 mice. These findings suggest that intestinal lipid metabolism is associated with susceptibility to obesity.

high fat; intestine; beta-oxidation; carnitine palmitoyltransferase; nicotinamide adenine dinucleotide phosphate+-dependent cytosolic malic enzyme



Address for reprint requests and other correspondence: H. Kondo, Biological Science Laboratories, Kao Corporation, 2606 Akabane, Ichikai-machi, Haga-gun, Tochigi 321–3497, Japan (e-mail: kondo.hidehiko{at}kao.co.jp)




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