title: Differential regulation of intestinal lipid metabolism-related genes in obesity-resistant A/J vs. obesity-prone C57BL/6J mice.
abstract: 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.
authors.affiliation: Biological Science Laboratories, Kao Corporation, Tochigi, Japan. kondo.hidehiko@kao.co.jp
authors.forename: Hidehiko
authors.initials: H
authors.lastname: Kondo
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Minegishi
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Komine
authors.forename: Takuya
authors.initials: T
authors.lastname: Mori
authors.forename: Ichiro
authors.initials: I
authors.lastname: Matsumoto
authors.forename: Keiko
authors.initials: K
authors.lastname: Abe
authors.forename: Ichiro
authors.initials: I
authors.lastname: Tokimitsu
authors.forename: Tadashi
authors.initials: T
authors.lastname: Hase
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Murase
mesh_terms: D000273:Adipose Tissue / Q000502:physiology; D000818:Animals; D002334:Carnitine O-Palmitoyltransferase / Q000235:genetics; D005227:Fatty Acids / Q000378:metabolism; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000502:physiology; D007328:Insulin / Q000097:blood; D007421:Intestine, Small / Q000502:physiology*; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism / Q000235:genetics*; D008099:Liver / Q000502:physiology; D008291:Malate Dehydrogenase / Q000235:genetics; D008297:Male; D051379:Mice; D008805:Mice, Inbred A; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D018482:Muscle, Skeletal / Q000502:physiology; D009765:Obesity / Q000235:genetics* / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013045:Species Specificity
chemical_list: D005227:Fatty Acids; D007328:Insulin; D020738:Leptin; D008291:Malate Dehydrogenase; C031917:malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+); D002334:Carnitine O-Palmitoyltransferase