1998 Fiscal Year Final Research Report Summary
The etiological importance of reduced B-cell masses for the development of type 2 diabetes mellitus.
| Project/Area Number |
09671061
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
内分泌・代謝学
|
|---|
| Research Institution | The University of Tokushima |
|---|
Principal Investigator |
SHIMA Kenji The University of Tokushima School of Medicine, Professor, 医学部, 教授 (90028407)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Takashi The University of Tokushima, School of Medicine, Instructor, 医学部, 助手 (40210009)
MIZUNO Akira The University of Tokushima Medical School Hospital, Instructor, 医学部附属病院, 助手 (80219641)
NOMA Yoshihiko The University of Tokushima Medical School Hospital, Lecturer, 医学部附属病院, 講師 (10218349)
KUWAJIMA Masamichi The University of Tokushima School of Medicine, Associate Professor, 医学部, 助教授 (00205262)
|
|---|
| Project Period (FY) |
1997 – 1998
|
| Keywords | Tvpe2DM / beta-cell proliferation / beta-cell mass / insulin secretion / insulin resistance / microangiopathy / fat droplet |
|---|
| Research Abstract |
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.
|
-
-
-
-
-
-
-
-
-
[Publications] Z.W.Man, M.Zhu, Y.Noma, K.Toide, T.Sato, Y.Asahi, T.Hirashima, S.Mori, K.Kawano, A.Mizuno, T.Sano and K.Shima: "Impaired beta-cell function and deposition of fat droplets in the pancrease as a consequence of hypertriglyceridemia in OLETF rat, a model of spontaneous NIDDM." Diabetes. 46. 1718-1724 (1997)
Description
「研究成果報告書概要(欧文)」より
-
-
-
