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首页> 外文期刊>American Journal of Physiology >Glucagon-like peptide-1 analog prevents obesity-related glomerulopathy by inhibiting excessive autophagy in podocytes
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Glucagon-like peptide-1 analog prevents obesity-related glomerulopathy by inhibiting excessive autophagy in podocytes

机译：胰高血糖素样肽-1个模拟通过抑制多粒细胞过量的自噬抑制肥胖相关的肾小球病

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摘要

To investigate the role of glucagon-like peptide-1 analog (GLP-1) in high-fat diet-induced obesity-related glomerulopathy (ORG). Male C57BL/6 mice fed a high-fat diet for 12 wk were treated with GLP-1 (200μg/kg) or 0.9% saline for 4 wk. Fasting blood glucose and insulin and the expression of podocin, nephrin, phosphoinositide 3-kinase (PI3K), glucose transporter type (Glut4), and microtubule-associated protein lA/lB-light chain 3 (LC3) were assayed. Glomerular morphology and podocyte foot structure were evaluated by periodic acid-Schiff staining and electron microscopy. Podocytes were treated with 150 nM GLP-1 and incubated with 400 μM palmitic acid (PA) for 12 h. The effect on autophagy was assessed by podocyte-speciflc Glut4 siRNA. Insulin resistance and autophagy were assayed by imniunofluorescence and Western blotting. The high-fat diet resulted in weight gain, ectopic glomerular lipid accumulation, increased insulin resistance, and fusion of podophyte foot processes. The decreased translocation of Glut4 to the plasma membrane and excess autophagy seen in mice fed a high-fat diet and in PA-treated cultured podocytes were attenuated by GLP-1. Podo-cyte-specific Glut4 siRNA promoted autophagy, and rapamycin-en-hanced autophagy worsened the podocyte injury caused by PA. Excess autophagy in podocytes was induced by inhibition of Glut4 translocation to the plasma membrane and was involved in the pathology of ORG. GLP-1 restored insulin sensitivity and ameliorated renal injury by decreasing the level of autophagy.
机译：探讨胰高血糖素样肽-1种族（GLP-1）在高脂肪饮食诱导的肥胖相关的肾小球病（ORG）中的作用。喂养高脂饮食12WK的雄性C57BL / 6小鼠用GLP-1（200μg/ kg）或0.9％盐水处理4周。测定空腹血糖和胰岛素和胰岛素，肾，磷酸亚膦腈3-激酶（PI3K），葡萄糖转运液（GLUT4）和微管相关蛋白LA / LB-轻链3（LC3）的表达。通过定期酸 - 席夫染色和电子显微镜评估肾小球形态和孔孔足部结构。用150nm GLP-1处理巨粒细胞，并与400μM棕榈酸（PA）温育12小时。通过Podocyte-ImpliclC Glut4 siRNA评估对自噬的影响。胰岛素抗性和自噬通过Imniunof荧光和蛋白质印迹测定。高脂饮食导致体重增加，异位肾小球脂质积累，增加的胰岛素抵抗力和富孔脚工艺的融合。通过GLP-1将Glut4与喂食高脂饮食和PA处理的培养的诱导的诱导的诱导的培养的诱导的培养的致鼠中的血浆膜和过量自噬的转移降低。通过GLP-1衰减。 PODO-Cyte特异性的Glut4 siRNA促进了自噬，雷帕霉素 - 脑卒中自噬令Pod细胞损伤造成的po。通过抑制Glut4易位与血浆膜来诱导过量自噬诱导，并参与org的病理学。通过降低自噬水平，GLP-1恢复胰岛素敏感性和改善肾损伤。

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