PDF(Pubmed)
Abstract：
High salt intake (HS) is associated with obesity and insulin resistance. ET-1, a peptide released in response to HS, inhibits the actions of insulin on cultured adipocytes through ET-1 type B (ETB) receptors; however, the in vivo implications of ETB receptor activation on lipid metabolism and insulin resistance is unknown. We hypothesized that activation of ETB receptors in response to HS intake promotes dyslipidemia and insulin resistance. In normal salt (NS) fed rats, no significant difference in body mass or epididymal fat mass was observed between control and ETB deficient rats. After 2 weeks of HS, ETB-deficient rats had significantly lower body mass and epididymal fat mass compared to controls. Nonfasting plasma glucose was not different between genotypes; however, plasma insulin concentration was significantly lower in ETB-deficient rats compared to controls, suggesting improved insulin sensitivity. In addition, ETB-deficient rats had higher circulating free fatty acids in both NS and HS groups, with no difference in plasma triglycerides between genotypes. In a separate experiment, ETB-deficient rats had significantly lower fasting blood glucose and improved glucose and insulin tolerance compared to controls. These data suggest that ET-1 promotes adipose deposition and insulin resistance via the ETB receptor.
摘要：
高盐摄入（HS）与肥胖和胰岛素抵抗有关。ET-1，一种响应HS释放的肽，通过ET-1B型（ETB）受体抑制胰岛素对培养的脂肪细胞的作用；然而，体内ETB受体激活对脂质代谢和胰岛素抵抗的影响尚不清楚.我们假设响应HS摄入而激活ETB受体促进血脂异常和胰岛素抵抗。在正常盐（NS）喂养的大鼠中，对照组和ETB缺乏大鼠之间的体重或附睾脂肪量没有显着差异。经过2周的HS，与对照组相比，缺乏ETB的大鼠的体重和附睾脂肪量明显较低。非空腹血糖在基因型之间没有差异；然而，与对照组相比，ETB缺乏大鼠的血浆胰岛素浓度显着降低，提示改善胰岛素敏感性。此外,在NS和HS组中，ETB缺乏的大鼠具有较高的循环游离脂肪酸，基因型之间的血浆甘油三酯没有差异。在一个单独的实验中，与对照组相比，ETB缺乏大鼠的空腹血糖显着降低，葡萄糖和胰岛素耐受性改善。这些数据表明ET-1通过ETB受体促进脂肪沉积和胰岛素抵抗。
