Improved glucose control and reduced body fat mass in free fatty acid receptor 2-deficient mice fed a high-fat diet

Improved glucose control and reduced body fat mass in free fatty acid receptor 2-deficient mice fed a high-fat diet
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DOI:
10.1152/ajpendo.00229.2010
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发表时间:
2011-01-01
影响因子:
5.1
通讯作者:
Bohlooly-Y, Mohammad
Bohlooly-Y, Mohammad
中科院分区:
医学2区
文献类型:
--
作者:
Bjursell, Mikael;Admyre, Therese;Bohlooly-Y, Mohammad

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[10]杨文辉,张文辉.在喂食高脂饮食的游离脂肪酸受体2缺陷小鼠中改善葡萄糖控制和减少体脂量。Am J Physiol Endocrinol Metab 300:E211-E220,2011.首次发表于2010年10月19日; doi:10.1152/ajpendo.00229.2010.-游离脂肪酸受体2(Ffar 2),也称为GPR 43,由短链脂肪酸(SCFA)激活,并在肠,脂肪细胞和免疫细胞中表达,表明参与脂质和免疫调节。在本研究中,给予Ffar 2缺陷型小鼠(Ffar 2-KO)高脂饮食(HFD)或普通饮食,并研究脂质和能量代谢。在HFD中,Ffar 2-KO小鼠具有较低的体脂量和增加的瘦体重。身体组成的改变伴随着血糖控制的改善和HOMA指数的降低,表明Ffar 2-KO小鼠的胰岛素敏感性改善。此外,Ffar 2-KO小鼠具有更高的能量消耗,伴随着更高的核心体温和增加的食物摄入。喂食HFD的Ffar 2-KO小鼠的肝脏重量和甘油三酯含量以及血浆胆固醇水平较低。组织学检查揭示了Ffar 2-KO小鼠棕色脂肪组织中散布的脂质减少。有趣的是,没有观察到白色脂肪组织(WAT)细胞大小的显著差异,但是与野生型小鼠相比,在来自HFD喂养的Ffar 2-KO的WAT中检测到显著更低的巨噬细胞含量。总之,Ffar 2缺陷至少部分地通过增加能量消耗来防止HFD诱导的肥胖和血脂异常。
Bjursell M, Admyre T, Goransson M, Marley AE, Smith DM, Oscarsson J, Bohlooly-Y M. Improved glucose control and reduced body fat mass in free fatty acid receptor 2-deficient mice fed a high-fat diet. Am J Physiol Endocrinol Metab 300: E211-E220, 2011. First published October 19, 2010; doi:10.1152/ajpendo.00229.2010.-Free fatty acid receptor 2 (Ffar2), also known as GPR43, is activated by short-chain fatty acids (SCFA) and expressed in intestine, adipocytes, and immune cells, suggesting involvement in lipid and immune regulation. In the present study, Ffar2-deficient mice (Ffar2-KO) were given a high-fat diet (HFD) or chow diet and studied with respect to lipid and energy metabolism. On a HFD, Ffar2-KO mice had lower body fat mass and increased lean body mass. The changed body composition was accompanied by improved glucose control and lower HOMA index, indicating improved insulin sensitivity in Ffar2-KO mice. Moreover, the Ffar2-KO mice had higher energy expenditure accompanied by higher core body temperature and increased food intake. The liver weight and content of triglycerides as well as plasma levels of cholesterol were lower in the Ffar2-KO mice fed a HFD. A histological examination unveiled decreased lipid interspersed in brown adipose tissue of the Ffar2-KO mice. Interestingly, no significant differences in white adipose tissue (WAT) cell size were observed, but significantly lower macrophage content was detected in WAT from HFD-fed Ffar2-KO compared with wild-type mice. In conclusion, Ffar2 deficiency protects from HFD-induced obesity and dyslipidemia at least partly via increased energy expenditure.