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蛋白质营养不良增强成年肥胖小鼠胰岛素分泌的放大途径。

Protein malnutrition potentiates the amplifying pathway of insulin secretion in adult obese mice.

机构信息

Department of Structural and Functional Biology, Institute of Biology, University of Campinas (UNICAMP), Campinas, SP, CEP: 13083-865, Brazil.

出版信息

Sci Rep. 2016 Sep 16;6:33464. doi: 10.1038/srep33464.

Abstract

Pancreatic beta cell (β) dysfunction is an outcome of malnutrition. We assessed the role of the amplifying pathway (AMP PATH) in β cells in malnourished obese mice. C57Bl-6 mice were fed a control (C) or a low-protein diet (R). The groups were then fed a high-fat diet (CH and RH). AMP PATH contribution to insulin secretion was assessed upon incubating islets with diazoxide and KCl. CH and RH displayed increased glucose intolerance, insulin resistance and glucose-stimulated insulin secretion. Only RH showed a higher contribution of the AMP PATH. The mitochondrial membrane potential of RH was decreased, and ATP flux was unaltered. In RH islets, glutamate dehydrogenase (GDH) protein content and activity increased, and the AMP PATH contribution was reestablished when GDH was blunted. Thus, protein malnutrition induces mitochondrial dysfunction in β cells, leading to an increased contribution of the AMP PATH to insulin secretion through the enhancement of GDH content and activity.

摘要

胰岛β细胞功能障碍是营养不良的结果。我们评估了营养过剩肥胖小鼠β细胞中放大通路(AMP PATH)的作用。将 C57Bl-6 小鼠喂食对照(C)或低蛋白饮食(R)。然后,这些组喂食高脂肪饮食(CH 和 RH)。用 diazoxide 和 KCl 孵育胰岛以评估 AMP PATH 对胰岛素分泌的贡献。CH 和 RH 表现出葡萄糖耐量降低、胰岛素抵抗和葡萄糖刺激的胰岛素分泌降低。只有 RH 显示出 AMP PATH 的更高贡献。RH 的线粒体膜电位降低,而 ATP 流量保持不变。在 RH 胰岛中,谷氨酸脱氢酶(GDH)蛋白含量和活性增加,并且当 GDH 被削弱时,AMP PATH 的贡献得以重建。因此,蛋白质营养不良导致β细胞线粒体功能障碍,通过增强 GDH 含量和活性,导致 AMP PATH 对胰岛素分泌的贡献增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa6b/5025848/6f04027290d6/srep33464-f1.jpg

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