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Cellular Physiology and molecular biology of amylin in NIDDM

NIDDM 中胰淀素的细胞生理学和分子生物学

基本信息

批准号：
07457226
负责人：
MATSUKURA Shigeru
金额：
$ 4.22万
依托单位：
Miyazaki Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1996
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07457226/
关键词：
amylin IAPP NIDDM islet amyloid 糖尿病

项目摘要

Amylin, also designated islet amyloid polypeptide, is a 37-amino acid peptide that was isolated from islet amyloid in 1987. The peptide is thought to be involved in the etiology of NIDDM by opposing insulin action in peripheral tissues and by destroying islet construction through amyloid deposition. We studied the properties of amylin, its synthesis and secretion in abnormal glucose tolerance, and amyloidogenesis of the islet in NIDDM.We developed three RIAs for amylin : human and rat common N-terminal region of amylin, and both human and rat C-terminal amylin. We also identified endogenous molecular forms of amylin in pancreata, gastrointestinal tracts and plasma of many mammals. Amylin messenger RNA whose size is 900 bases is predminantly expressed in the pancreas. Amylin is detected in rat fetal pancreas, and its content gradually increases during development. Amylin in the antrum appears 3 days after birth. In the human pancreas, amylin is detected at 15 weeks of gestation. Pancreatic amylin content was 221.6<plus-minus>78.2 pmol/g wet weight in man and 328.5<plus-minus>25.0 pmol/g wet weight in rat, being approximately 1-2% of insulin content. Basal plasma immunoreactive amylin level in normal individuals was 2.4-5.8 fmol/ml, being increased in subjects with ovesity or impaired glucose tolerance, and decreased in diabetic patients. Amylin was co-secreted with insulin in physiological conditiIslet amyloid deposition is not responsible for the primary etiology of NIDDM,however, the amyloid deposits could intensify islet dysfunction and contribute to the progression of NIDDM.

胰淀素又称胰岛淀粉样多肽，是1987年从胰岛淀粉样蛋白中分离得到的一种由37个氨基酸组成的多肽。这种多肽被认为与NIDDM的病因学有关，它通过对抗外周组织中的胰岛素作用，并通过淀粉样蛋白沉积破坏胰岛结构。我们研究了胰淀素的性质、糖耐量异常时胰淀素的合成和分泌以及胰岛淀粉样蛋白的形成。我们建立了三个胰淀素的RIA：人和大鼠共同的胰淀素N-末端区域和人和大鼠的C-末端胰淀素。我们还在许多哺乳动物的胰腺、胃肠道和血浆中发现了内源性淀粉素的分子形式。胰淀素信使RNA的大小为900个碱基，主要在胰腺中表达。胰淀素存在于大鼠胚胎胰腺中，随着胚胎发育，胰淀素含量逐渐增加。胃窦内的胰淀素在出生后3天出现。在人的胰腺中，胰淀素在怀孕15周时被检测到。人胰腺胰淀素含量为221.6±78.2pmol/g湿重，大鼠为328.5±25.0pmol/g湿重，约为胰岛素含量的1-2%。正常人基础血浆免疫反应性胰淀素水平为2.4~5.8fmol/ml，肥胖或糖耐量低减患者血浆免疫反应性胰淀素水平升高，糖尿病患者下降。胰岛淀粉样沉积不是NIDDM的主要病因，但可加重胰岛功能障碍，促进NIDDM的发展。