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Adipocyte Metabolism in Adipocyte Fatty Acid Bindign Protein Knockout (aP2~-/-) Mice After Short-Term High-Fat Feeding

机译:短期高脂喂养后脂肪细胞脂肪酸结合蛋白基因敲除(aP2〜-/-)小鼠的脂肪细胞代谢

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摘要

Mice null for adipocyte fatty acid binding protein (AFABP) compensate by increasing expression of ker- atinocyte fatty acid binding protein (KFABP) (Hotamis- ligil et al. Science 274:1377-1397, 1996). In the present study, AFABP knockout 9KO) and wild-type (WT) mice became equally obese on a high-fat diet, as judged by fat pad weights, adipocyte size, and body composition analysis. High-fat feeding led to moderate insulin resistance in both WT and AFABP knockout mice, as indicated by an ~2-fold increase in plasma insulin.
机译:通过增加角化细胞脂肪酸结合蛋白(KFABP)的表达来补偿缺乏脂肪细胞脂肪酸结合蛋白(AFABP)的小鼠(Hotamisligil等,Science 274:1377-1397,1996)。在本研究中,AFABP基因敲除9KO)和野生型(WT)小鼠在高脂饮食下同样肥胖,这是通过脂肪垫重量,脂肪细胞大小和身体成分分析来判断的。高脂喂养在WT和AFABP基因敲除小鼠中均引起中等程度的胰岛素抵抗,这是血浆胰岛素增加约2倍的结果。

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