消化管ホルモン産生細胞の管腔側表面に存在する食品成分受容機構の解明
| Project/Area Number |
02660093
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
応用生物化学・栄養化学
|
|---|
| Research Institution | Kyoto University |
|---|
Principal Investigator |
FUSHIKI Tohru Kyoto Univ., Food Science & Technology, Assistant Professor, 農学部, 助教授 (20135544)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
INOUE Kazuo Kyoto Univ., Food Scinece & Technology, Assistant Professor, 農学部, 助手 (80213148)
KAWADA Teruo Kyoto Univ., Food Science & Technology, 農学部, 助手 (10177701)
|
|---|
| Project Period (FY) |
1990 – 1991
|
| Project Status |
Completed (Fiscal Year 1991)
|
| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1990: ¥1,400,000 (Direct Cost: ¥1,400,000)
|
|---|
| Keywords | GIP / Gastrointestinal hormone / Glucose senser / Sweet taste / Gymnemic acid / duodenum / portal vein / glucose / グルコ-スセンサ- / グルコ-ス / 消化管ホルモン産生細胞 / コレシストキニン / 食物刺激 / ホルモン分泌 |
|---|
| Research Abstract |
Gastric inhibitory polypetide(GIP)-release into the portal vein in response to duodenal infusion of D-glucose was studied as a model for the gastrointestinal hormone release by food components. Intraduodenal infusion of D-glucose(16.68 and 8.34 mmol/kg/hr)significantly increased the portal immunoreactive GIP(IR-GIP)level, there being a dose-response relationship. Fructose, glycine and stevioside in dose of 16.68 mmol/kg/hr(infusion rate, 0.5 ml/kg/min)did not increase the portal IR-GIP level. The increase in the portal IR-GIP induced by glucose was significantly depressed by concomitantly infused leai extract of Gymnema sylvestre, purified gymnemic acid(30mg/kg/hr)and phlorizin(0.15 mmol/kg/hr), but not markedly depressed by cytochalasin B(1.5 mg/kg/hr). 3-o-Methylglucose and 2-deoxyglucose(16.68mmol/kg/hr)did not cause any significant IR-GIP release. Glybenclamide(3 mg/kg/hr), which causes the closure of the K^+channels and induces insulin-release in the pancreatic beta-cell, mannohepturose(0.12 mmol/kg/hr), which inhibits glycolysis, and procain and lidocain(1%), which inhibit the vagal glucoreceptor in the lumen, did not affect the portal IR-GIP level. From these results it would appear that(1)a glucose receptor, which interacts with the leaf extract of Gymnema sylvestre, purified gymnemic acid and phlorizin, but not fructose or 3-o-methylglucose, exists for the release of IR-GIP, (2)the intracellular signal for GIP release may not be transducted via the ATP-sensitive K^+ channels, which was proposed for the insulin-release from -cells, (3)and the glucose receptor for GIP release is unlikely identical with a glucose transporter or a vagal glucoreceptor in the lumen.
|
Report
(3 results)
Research Products
(3 results)
