Differential regulation of intestinal lipid metabolism-related genes in obesity-resistant A/J vs. obesity-prone C57BL/6J mice
Differential regulation of intestinal lipid metabolism-related genes in obesity-resistant A/J vs. obesity-prone C57BL/6J mice
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DOI：
10.1152/ajpendo.00583.2005
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发表时间：
2006-11-01
影响因子：
5.1
通讯作者：
Murase, Takatoshi
中科院分区：
文献类型：
--
作者：
Kondo, Hidehiko;Minegishi, Yoshihiko;Murase, Takatoshi
以肥胖抵抗的A/J小鼠和肥胖倾向的C57BL/6J(B6)小鼠为研究对象，研究了高脂喂养对小鼠小肠基因表达的影响。两个品系的小鼠都以低脂(LF；5%脂肪)或HF(30%脂肪)饲料喂养2wk。定量逆转录-聚合酶链式反应分析显示，两个品系小鼠的脂肪代谢相关基因，包括肉碱棕榈酰基转移酶(CPT)I、肝脏脂肪酸结合蛋白、丙酮酸脱氢酶-4和NADP(+)依赖的胞浆苹果酸酶，在HF喂养后均上调。A/J小鼠上调的基因表达水平高于B6小鼠，提示A/J小鼠小肠脂肪代谢更为活跃。脂质代谢相关基因的显著上调是针对小肠的；在肝脏、肌肉和白色脂肪组织中的表达水平很低或没有变化。与肥胖倾向B6小鼠相比，HF喂养可提高A/J小鼠的苹果酸酶、CPT和β-氧化活性，上调的苹果酸酶和CPT活性显著高于肥胖倾向的B6小鼠。这些发现表明，肠道脂肪代谢与肥胖易感性有关。
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.