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

胃抑制多肽（GIP）释放到门静脉响应十二指肠灌注D-葡萄糖作为模型的胃肠激素释放的食物成分进行了研究。十二指肠内灌注D-葡萄糖（16.68和8.34 mmol/kg/hr）可显著增加门脉免疫反应GIP（IR-GIP）水平，并存在剂量-反应关系。果糖、甘氨酸和甜菊苷的剂量为16.68 mmol/kg/hr（输注速率为0.5 ml/kg/min），未增加门静脉IR-GIP水平。同时输注匙羹藤叶提取物、纯化匙羹藤酸（30 mg/kg/hr）和根皮苷（0.15 mmol/kg/hr）可显著抑制葡萄糖诱导的门脉IR-GIP的增加，但细胞松弛素B（1.5 mg/kg/hr）不显著抑制。3-O-甲基葡萄糖和2-脱氧葡萄糖（16.68mmol/kg/hr）未引起任何显著的IR-GIP释放。格列本脲（3 mg/kg/hr）可导致K^+通道关闭并诱导胰腺β细胞释放胰岛素，甘露庚酮糖（0.12 mmol/kg/hr）可抑制糖酵解，普鲁卡因和利多卡因（1%）可抑制管腔中的迷走神经葡萄糖受体，这些药物均不影响门静脉IR-GIP水平。从这些结果可以看出：（1）IR-GIP的释放存在一种葡萄糖受体，它与匙羹藤叶提取物、纯化匙羹藤酸和根皮苷相互作用，但不与果糖或3-O-甲基葡萄糖相互作用;（2）GIP释放的细胞内信号可能不通过ATP敏感的K^+通道进行转导，而ATP敏感的K^+通道被认为是细胞释放胰岛素的通道，（3）GIP释放的葡萄糖受体不太可能与管腔中的葡萄糖转运蛋白或迷走神经葡萄糖受体相同。

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.