Sykes S, Morgan L M, English J, Marks V
J Endocrinol. 1980 May;85(2):201-7. doi: 10.1677/joe.0.0850201.
A rat intestinal perfusion technique has been used to assess the ability of a number of monosaccharides, monosaccharide analogues and disaccharides to stimulate intestinal release of immunoreactive gastric inhibitory polypeptide (GIP). Perfusates containing glucose, sucrose, galactose, maltose, 3-O-methylglucose or alpha- or beta- methylglucoside at concentrations of 100 mmol/l in Krebs-Ringer phosphate buffer (KRP) produced significant stimulation of GIP release compared with the control perfusions with KRP alone (P less than 0.02). Mannose, 6-deoxygalactose, 2-deoxyglucose, myoinositol, fructose or lactose (100 mmol/l of each) did not stimulate GIP release compared with controls. There was no significant difference in the ability of sucrose, maltose or beta-methylglucoside (100 mmol/l of ach) to release GIP compared with 100 mmol glucose/l, but galactose, 3-O-methylglucose and alpha-methylglucoside (100 mmol/l of each) produced significantly lower GIP responses than did glucose (P less than 0.02). Addition of 5 mmol phloridzin/l to a perfusate containing 50 mmol glucose/l prevented intestinal absorption of glucose and abolished the GIP response. The molecular configuration of monosaccharides which have the ability to stimulate GIP release agreed well with the structural requirements for active transport by the sodium-dependent hexose pathway.
一种大鼠肠道灌注技术已被用于评估多种单糖、单糖类似物和二糖刺激肠道释放免疫反应性胃抑制多肽（GIP）的能力。与仅用Krebs-Ringer磷酸盐缓冲液（KRP）进行的对照灌注相比，在KRP中含有浓度为100 mmol/l的葡萄糖、蔗糖、半乳糖、麦芽糖、3-O-甲基葡萄糖或α-或β-甲基葡萄糖苷的灌注液能显著刺激GIP释放（P<0.02）。与对照相比，甘露糖、6-脱氧半乳糖、2-脱氧葡萄糖、肌醇、果糖或乳糖（各100 mmol/l）不刺激GIP释放。与100 mmol/l葡萄糖相比，蔗糖、麦芽糖或β-甲基葡萄糖苷（各100 mmol/l）释放GIP的能力没有显著差异，但半乳糖、3-O-甲基葡萄糖和α-甲基葡萄糖苷（各100 mmol/l）产生的GIP反应明显低于葡萄糖（P<0.02）。向含有50 mmol/l葡萄糖的灌注液中添加5 mmol/l根皮苷可阻止肠道对葡萄糖的吸收并消除GIP反应。具有刺激GIP释放能力的单糖的分子构型与钠依赖性己糖途径主动转运的结构要求非常吻合。
