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C肽对肾脏生理和糖尿病的影响。

C-Peptide effects on renal physiology and diabetes.

作者信息

Rebsomen L, Khammar A, Raccah D, Tsimaratos M

机构信息

UPRES EA 21-93, Laboratoire de Diabétologie, Faculté de Médecine de Marseille, Université de la Méditerranée, 13385 Marseille Cedex 05, France.

出版信息

Exp Diabetes Res. 2008;2008:281536. doi: 10.1155/2008/281536.

DOI:10.1155/2008/281536
PMID:18509500
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2396455/
Abstract

The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability to stimulate the Na,K-ATPase activity. Precisely, the C-peptide reduces diabetes-induced glomerular hyperfiltration both in animals and humans, therefore, resulting in regression of fibrosis. The tubular function is also concerned as diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with the reduction of the diabetes-induced glomerular hyperfiltration. The tubular effectors of C-peptide were considered to be tubule transporters, but recent studies have shown that biochemical pathways involving cellular kinases and inflammatory pathways may also be important. The matter theory concerning the C-peptide effects is a metabolic one involving the effects of the C-peptide on lipidic metabolic status. This review concentrates on the most convincing data which indicate that the C-peptide is a biologically active hormone for renal physiology.

摘要

胰岛素原的C肽对胰岛素的生物合成很重要,长期以来一直被认为是无生物活性的。动物研究表明,C肽的一些肾脏效应部分可以通过其刺激钠钾ATP酶活性的能力来解释。确切地说,C肽在动物和人类中均可减轻糖尿病诱导的肾小球高滤过,从而导致纤维化消退。肾小管功能也受到关注,因为补充C肽的糖尿病动物表现出更好的肾功能,导致尿钠排泄和蛋白质排泄减少,同时糖尿病诱导的肾小球高滤过也有所减轻。C肽的肾小管效应器曾被认为是肾小管转运体,但最近的研究表明,涉及细胞激酶和炎症途径的生化途径可能也很重要。关于C肽作用的物质理论是一种涉及C肽对脂质代谢状态影响的代谢理论。本综述集中于最有说服力的数据,这些数据表明C肽是一种对肾脏生理学具有生物活性的激素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e33/2396455/424f83de0b3c/EDR2008-281536.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e33/2396455/424f83de0b3c/EDR2008-281536.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e33/2396455/424f83de0b3c/EDR2008-281536.001.jpg

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Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists attenuate the profibrotic response induced by TGF-beta1 in renal interstitial fibroblasts.过氧化物酶体增殖物激活受体γ(PPAR-γ)激动剂可减弱转化生长因子β1(TGF-β1)在肾间质成纤维细胞中诱导的促纤维化反应。
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Proinsulin C-peptide abrogates type-1 diabetes-induced increase of renal endothelial nitric oxide synthase in rats.胰岛素原C肽可消除1型糖尿病诱导的大鼠肾内皮型一氧化氮合酶增加。
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Proinsulin C-peptide constricts glomerular afferent arterioles in diabetic mice. A potential renoprotective mechanism.
利用毕赤酵母表达系统表达和纯化含C肽的胰岛素
Biomed Res Int. 2016;2016:3423685. doi: 10.1155/2016/3423685. Epub 2016 Aug 4.
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Pathophysiology of the diabetic kidney.糖尿病肾病的病理生理学。
Compr Physiol. 2011 Jul;1(3):1175-232. doi: 10.1002/cphy.c100049.
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Low-cost production of proinsulin in tobacco and lettuce chloroplasts for injectable or oral delivery of functional insulin and C-peptide.在烟草和生菜叶绿体中低成本生产胰岛素原,用于注射或口服递送功能性胰岛素和 C 肽。
Plant Biotechnol J. 2011 Jun;9(5):585-98. doi: 10.1111/j.1467-7652.2010.00582.x. Epub 2010 Dec 8.
6
Proinsulin C-peptide antagonizes the profibrotic effects of TGF-beta1 via up-regulation of retinoic acid and HGF-related signaling pathways.胰岛素原C肽通过上调视黄酸和肝细胞生长因子相关信号通路来拮抗转化生长因子-β1的促纤维化作用。
Mol Endocrinol. 2010 Apr;24(4):822-31. doi: 10.1210/me.2009-0391. Epub 2010 Mar 2.
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The renal vascular response to diabetes.糖尿病的肾脏血管反应。
Curr Opin Nephrol Hypertens. 2010 Jan;19(1):85-90. doi: 10.1097/MNH.0b013e32833240fc.
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