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The etiological importance of reduced B-cell masses for the development of type 2 diabetes mellitus.

B 细胞质量减少对于 2 型糖尿病发生的病因学重要性。

基本信息

批准号：
09671061
负责人：
SHIMA Kenji
金额：
$ 1.98万
依托单位：
The University of Tokushima
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09671061/
关键词：
Tvpe2DM beta-cell proliferation beta-cell mass insulin secretion insulin resistance microangiopathy fat droplet OLETF LETO 部分膵切除 β細胞増殖能胎児ラ氏島様細胞集塊 β細胞量膵管上皮細胞 β細胞インスリン含量

项目摘要

In this study, we tried to explore whether an impairment of insulin secretion observed in type 2 diabetes mellitus is caused by the reduction of beta -cell mass using OLETF rats, a model of type 2 diabetes. The following results have been obtained ;1. A failure in the compensative proliferation of pancreatic beta-cells has been reported in the OLETF rat. The present study was undertaken to define whether the defect is involved in its fetal model. The defective morphogenesis of endocrine cells and functional adaptation to increased metabolic demand could be thought of as a failure involved in the fetal model, and a decreased expression of PDX- 1 may be one of the factors which contribute to this failure in this model rat.2. Hypertriglyceridemia resulted in significant TG stores in the islets, which subsequently inhibited glucose-induced insulin secretion, at least in part, via reduced glucokinase activity in the islets Fat droplets in the islets may play an important role in hastening the development of diabetes mellitus in this rat model.3. The fine capillaries that form a network in the islets were extremely sparse in the OLETF rat, resulting in a defective glomerular-like configuration, whereas those from the control rat (LETO) were dense, forming a nearlv typical glomerular-like configuration.4. Wistar fatty rat, another type 2 model, has a poor capacity for proliferation of pancreatic beta -cells, which causes the onset of overt diabetes along with insulin resistance due to extreme obesity just like OLETF rats.

在本研究中，我们试图探索在2型糖尿病中观察到的胰岛素分泌障碍是否是由使用OLETF大鼠（2型糖尿病模型）的β细胞质量减少引起的。取得了以下成果：1.据报道，OLETF大鼠中胰腺β细胞代偿性增殖失败。本研究是为了确定缺陷是否涉及其胎儿模型。内分泌细胞的形态发生缺陷和对代谢需求增加的功能适应可以被认为是胎儿模型中涉及的失败，并且PDX- 1的表达降低可能是导致该模型大鼠中这种失败的因素之一。高甘油三酯血症导致胰岛中显著的TG储存，其随后至少部分地通过降低胰岛中的葡萄糖激酶活性来抑制葡萄糖诱导的胰岛素分泌。胰岛中的脂肪滴可能在加速该大鼠模型中糖尿病的发展中起重要作用。OLETF大鼠胰岛中形成网络的细小毛细血管非常稀疏，导致有缺陷的肾小球样构型，而对照大鼠（LETO）的毛细血管密集，形成近典型的肾小球样构型.另一种2型模型Wistar肥胖大鼠胰腺β-细胞增殖能力差，这导致明显的糖尿病沿着由于极度肥胖引起的胰岛素抵抗的发作，就像OLETF大鼠一样。