| Project/Area Number |
11671109
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Metabolomics
|
|---|
| Research Institution | International Medical Center of Japan (2000-2001)
Chiba University (1999) |
|---|
Principal Investigator |
YASUDA Kazuki International Medical Center of Japan, Research Institute, Director, 代謝疾患研究部, 部長 (80311611)
|
|---|
| Project Period (FY) |
1999 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
|---|
| Keywords | pancreatic beta cells / fatty acid / differential display / microarray / glutamate dehydrogenase / 遺伝子発現 / GeneChipシステム / デファレンシャルディスプレイ |
|---|
| Research Abstract |
Using mouse pancreatic beta cell line, beta HC9 cells, we first demonstrated that major isoform of FATP (fatty acid transport protein) expressed was FATP4, and no novel isoform was found for ACBP (acyl-CoA binding protein). We then tried to identify genes whose expression was differentially regulated by 1mM palmitate treatment for 72 hours which resulted in the enhanced glucose-induced insulin secretion. We applied two comprehensive methods, namely, fluorescent differential display (FDD ; HIEROGLYPH, GENOMYX, Inc) and DNA microarray (GeneChip system, Affymetrix, Inc). Although the results did not have an overlap, altogether we obtained more than 100 lipid-responsive genes, including novel ones. We also identified a Japanese case of hyperinsulinism with hyperammonemia (HI-HA syndrome) due to an activating mutation in the glutamate dehydrogenase gene. The pathophysiology was of great interest as the interplay of amino acid metabolism and glucose homeostasis.
|
