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钙蛋白酶系统与糖尿病

The calpain system and diabetes.

作者信息

Pandurangan Muthuraman, Hwang Inho, Orhirbat Chinzorio, Jieun Yang, Cho Soo-Hyun

机构信息

Department of Biomedical Engineering, Dongguk University, Seoul, South Korea.

Department of Animal Science and BK21 PLUS program, Chonbuk National University, Jeonju, South Korea.

出版信息

Pathophysiology. 2014 Jun;21(2):161-7. doi: 10.1016/j.pathophys.2014.01.003. Epub 2014 Mar 14.

DOI:10.1016/j.pathophys.2014.01.003
PMID:24630865
Abstract

Diabetes mellitus is recognized as a clinical syndrome that is characterized by hyperglycemia due to deficiency of insulin. The global prevalence of diabetes has been estimated to increase from 4% (1995) to 5.4% by the year 2025. Insulin dependent diabetes mellitus (IDDM/Type-1) in human, generating hyperglycemia due to insulin deficiency as a consequence of destructing beta cells in the pancreatic islets. Non-insulin dependent diabetes mellitus (NIDDM/Type-II), is a multifactorial, exact biochemical and genetic defect which has not yet been elucidated completely. Calpains seem to play a role in NIDDM and IDDM. Positional cloning experiments revealed that there is a NIDDM susceptibility to calpain 10 (CAPN10). Increased calpain activity and leukocyte trafficking were noticed in the microcirculation in ZDF (Zuker diabetic fatty) rats. Exercise and low body weight play a significant role in reducing calpains expression or elevating the calpains degradation in the skeletal muscle of NIDDM rats. Numerous investigations have been reported that non-coding polymorphisms in CAPN10 proteins might be involved in the NIDDM. Calpain and its mRNA presence had been reported in tissues from many mammalian species. CAPN10 and other calpains seem to be linked to glucose metabolism, insulin secretion and action pathways. This review will give an overview of the role of calpain in NIDDM and IDDM.

摘要

糖尿病被认为是一种临床综合征,其特征是由于胰岛素缺乏导致血糖升高。据估计,全球糖尿病患病率将从1995年的4%增加到2025年的5.4%。人类胰岛素依赖型糖尿病(IDDM/1型),由于胰岛β细胞被破坏导致胰岛素缺乏而产生高血糖。非胰岛素依赖型糖尿病(NIDDM/2型)是一种多因素、确切的生化和遗传缺陷,尚未完全阐明。钙蛋白酶似乎在NIDDM和IDDM中起作用。定位克隆实验表明,钙蛋白酶10(CAPN10)存在NIDDM易感性。在ZDF( Zucker糖尿病肥胖)大鼠的微循环中发现钙蛋白酶活性增加和白细胞运输。运动和低体重在降低NIDDM大鼠骨骼肌中钙蛋白酶的表达或提高其降解方面起着重要作用。许多研究报告称,CAPN10蛋白中的非编码多态性可能与NIDDM有关。在许多哺乳动物物种的组织中都报道了钙蛋白酶及其mRNA的存在。CAPN10和其他钙蛋白酶似乎与葡萄糖代谢、胰岛素分泌和作用途径有关。本综述将概述钙蛋白酶在NIDDM和IDDM中的作用。

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The calpain system and diabetes.钙蛋白酶系统与糖尿病
Pathophysiology. 2014 Jun;21(2):161-7. doi: 10.1016/j.pathophys.2014.01.003. Epub 2014 Mar 14.
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Do non-insulin-dependent diabetes mellitus (NIDDM) and insulin-dependent diabetes mellitus (IDDM) share genetic susceptibility loci? An analysis of putative IDDM susceptibility regions in familial NIDDM.非胰岛素依赖型糖尿病(NIDDM)和胰岛素依赖型糖尿病(IDDM)是否共享遗传易感性位点?对家族性NIDDM中假定的IDDM易感性区域的分析。
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On the pathophysiology of late onset non-insulin dependent diabetes mellitus. Current controversies and new insights.关于晚发型非胰岛素依赖型糖尿病的病理生理学。当前的争议与新见解。
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Type 2 diabetes candidate gene CAPN10: first, but not last.2型糖尿病候选基因钙蛋白酶10:首个,但并非最后一个。
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Studies of gene expression and activity of hexokinase, phosphofructokinase and glycogen synthase in human skeletal muscle in states of altered insulin-stimulated glucose metabolism.胰岛素刺激的葡萄糖代谢改变状态下人体骨骼肌中己糖激酶、磷酸果糖激酶和糖原合酶的基因表达及活性研究。
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Low mitochondrial glycerol phosphate dehydrogenase and pyruvate carboxylase in pancreatic islets of Zucker diabetic fatty rats.Zucker糖尿病肥胖大鼠胰岛中线粒体甘油磷酸脱氢酶和丙酮酸羧化酶水平较低。
Diabetes. 1996 Nov;45(11):1626-30. doi: 10.2337/diab.45.11.1626.

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Therapeutic potential of cyanobacteria against streptozotocin-induced diabetic rats.蓝藻细菌对链脲佐菌素诱导的糖尿病大鼠的治疗潜力。
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