2006 Fiscal Year Final Research Report Summary
Study of impaired insulin exocytosis in diabetes mellitus by imaging technique
| Project/Area Number |
15390108
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | Kyorin University |
|---|
Principal Investigator |
NAGAMATSU Shinya Kyorin University, School of Medicine, Professor, 医学部, 教授 (80231489)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
OHARA Mica (IMAIZUMI Mica) Kyorin University, School of Medicine, Associate Professor, 医学部, 助教授 (40201941)
WATANABE Takeshi Kyorin University, School of Medicine, Professor, 医学部, 教授 (00191768)
|
|---|
| Project Period (FY) |
2003 – 2006
|
| Keywords | Insulin / TIRF / exocytosis / imaging / pancreatic β cell / diabetes mellitus / insulin secretion |
|---|
| Research Abstract |
In these years the number of diabetic patients significantly increased worldwide and caused cerebrovascular disorder and heart vascular events, therefore, the onset prevention and restricted blood sugar levels control of diabetic patients are regarded as urgent business for both human health and medical economy. Because impaired insulin release is characteristics in type 2 diabetes, to elucidate the mechanism of normal and impaired insulin exocytosis is important. In this study, we developed the imaging system of total internal reflection fluorescence(TIRF) and applied this imaging system to pancreatic beta cells. Our system is a powerful tool for disclosure of insulin docking and fusion system by monitoring the dynamic motion of insulin granules on the plasma membrane. We found that granules fusing during the first phase insulin release originated mostly from morphologically previously docked granules, whereas granules fusing during the second phase arose from newcomers that were originally stored intracellulary. We also found that previously docked granules were colocalized with syntaxin 1A clusters in the plasma membrane, and fused from them. Finally we found that in diabetic beta cells, syntaxin 1A clusters decreased, thereby, docked granules decreased, as a result, first phase of insulin release decreased in the diabetic status.
|
-
-
[Journal Article] Elevation of the post-translational modification of proteins by 0-linked N-acetylglucosamine leads to deterioration of the glucose-stimulated insulin secretion in the pancreas of diabetic Goto-Kakizaki rats.2007
Author(s)
Akimoto Y, Hart GW, Wells L, Vosseller K, Yamamoto K, Munetomo E, Ohara-Imaizumi M, Nishiwaki C, Nagamatsu S, Hirano H, Kawakami H
-
Journal Title
Glycobiology.Feb 17(2)
Pages: 127-140
Description
「研究成果報告書概要(欧文)」より
-
[Journal Article] Protein kinase C delta plays a non-redundant role in insulin secretion in pancreatic beta cells.2007
Author(s)
Uchida T, Iwashita N, Ohara-Imaizumi M, Ogihara T, Nagai S, Choi JB, Tamura Y, Tada N, Kawamori R, Nakayama KI, Nagamatsu S, Watada H
-
Journal Title
J Biol Chem 282(4)
Pages: 2707-2716
Description
「研究成果報告書概要(欧文)」より
-
-
-
-
-
-
-
