Department of Biological Sciences, University of Warwick, Coventry, UK. C.Hills @ warwick.ac.uk
Am J Nephrol. 2010;31(5):389-97. doi: 10.1159/000289864. Epub 2010 Mar 31.
BACKGROUND/AIMS: Insulin is synthesised as a pro-hormone with an interconnecting C-peptide, cleaved during post-translational modification. This review discusses growing evidence which indicates that C-peptide is biologically active, benefiting microvascular complications associated with diabetes.
To explore the renoprotective role of C-peptide in diabetic nephropathy (DN), we reviewed the literature using PubMed for English language articles that contained key words related to C-peptide, kidney and DN.
Numerous studies have demonstrated that C-peptide ameliorates a number of the structural and functional renal disturbances associated with uncontrolled hyperglycaemia in human and animal models of type 1 diabetes mellitus that lead to the development and progression of nephropathy, including abrogation of glomerular hyperfiltration, reduced microalbuminuria, decreased mesangial expansion and increased endothelial nitric oxide synthase levels. The in vitro exposure of kidney proximal tubular cells to physiological concentrations of C-peptide activates extracellular signal-regulated kinase, phosphatidylinositol 3-kinase, protein kinase C, elevates intracellular calcium, and stimulates transcription factors NF-kappaB and peroxisome proliferator-activated receptor-gamma.
Burgeoning studies suggest that C-peptide is more than merely a link between the A and B chains of the proinsulin molecule and represents a future therapeutic tool in reducing complications of DN.
背景/目的：胰岛素作为一种前激素合成，具有连接的 C 肽，在翻译后修饰过程中被切割。这篇综述讨论了越来越多的证据表明 C 肽具有生物活性，可改善与糖尿病相关的微血管并发症。
为了探讨 C 肽在糖尿病肾病（DN）中的肾保护作用，我们使用 PubMed 检索了英文文献，其中包含与 C 肽、肾脏和 DN 相关的关键词。
大量研究表明，C 肽可改善 1 型糖尿病患者和动物模型中不受控制的高血糖引起的多种结构和功能肾损伤，从而导致肾病的发生和进展，包括肾小球高滤过、微量白蛋白尿减少、系膜扩张减少和内皮型一氧化氮合酶水平升高。在体外将肾脏近端小管细胞暴露于生理浓度的 C 肽可激活细胞外信号调节激酶、磷脂酰肌醇 3-激酶、蛋白激酶 C，升高细胞内钙，并刺激转录因子 NF-κB 和过氧化物酶体增殖物激活受体-γ。
新兴研究表明，C 肽不仅仅是前胰岛素分子 A 和 B 链之间的连接物，而且是减少 DN 并发症的未来治疗工具。
