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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

阐明胃肠激素产生细胞管腔表面的食物成分受体机制

基本信息

批准号：
02660093
负责人：
FUSHIKI Tohru
金额：
$ 1.41万
依托单位：
Kyoto University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1991
项目状态：
已结题

项目摘要

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.

以胃抑制多肽(GIP)释放到门静脉对十二指肠输注D-葡萄糖的反应作为食物成分释放胃肠激素的模型。十二指肠内注射D-葡萄糖(16.68和8.34 mmol/kg/hr)可显著增加门静脉免疫反应性GIP(IR-GIP)水平，并存在剂量-反应关系。果糖、甘氨酸和甜菊糖苷16.68 mmol/kg/hr(输液速率0.5ml/kg/min)不能增加门静脉IR-GIP水平。联合应用生藤提取物、葛根素(0.15 mg/kg/hr)和葛根素(0.15 mg/kg/hr)可显著抑制葡萄糖诱导的门静脉IR-GIP升高，而细胞松弛素B(1.5 mg/kg/hr)对此无明显抑制作用。3-O-甲基葡萄糖和2-脱氧葡萄糖(16.68 mmol/kg/hr)对IR-GIP释放无明显影响。阻断K~+通道并诱导胰岛β细胞胰岛素释放的格列本脲(3 mg/kg/hr)、抑制糖酵解的甘露七糖(0.12 mmol/kg/hr)、抑制管腔内迷走神经糖感受器的普鲁卡因和利多卡因(1%)对门静脉IR-GIP水平无影响。从这些结果可以看出：(1)释放IR-GIP的葡萄糖受体不与果糖或3-O-甲基葡萄糖相互作用，而是与绞股蓝叶提取物、提纯的裸子酸和根茎苷相互作用；(2)细胞内释放GIP的信号可能不通过细胞释放胰岛素的ATP敏感的K~+通道传递；(3)释放GIP的葡萄糖受体不太可能与管腔内的葡萄糖转运体或迷走神经糖受体相同。