| 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)
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| 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.
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