Nakanome C, Akai H, Umezu M, Toyota T, Goto Y
Tohoku J Exp Med. 1983 Mar;139(3):287-92. doi: 10.1620/tjem.139.287.
Plasma gastric inhibitory polypeptide (GIP) concentrations following an oral glucose load were measured in 27 diabetics and 10 normal subjects. Plasma GIP concentrations increased significantly from the mean basal value following an oral glucose load in both groups. Diabetics showed significantly higher levels of plasma GIP in association with delayed and diminished peak increases in plasma insulin levels. When diabetics were divided into two groups according to their basal levels of blood glucose, moderate and severe diabetics exhibited more exaggerated increments of plasma GIP than mild diabetics. This exaggerated GIP response to an oral glucose load in proportion to the glucose intolerance indicates a relative failure of the beta cell response to GIP in diabetics and that the mechanism involved in hypersecretion of GIP would be diminution of the inhibition of GIP release caused by insulin in diabetics.
对27名糖尿病患者和10名正常受试者口服葡萄糖负荷后血浆胃抑制性多肽（GIP）浓度进行了测定。两组口服葡萄糖负荷后，血浆GIP浓度均较平均基础值显著升高。糖尿病患者血浆GIP水平显著更高，同时血浆胰岛素水平的峰值升高延迟且降低。根据糖尿病患者的基础血糖水平将其分为两组时，中度和重度糖尿病患者血浆GIP的升高比轻度糖尿病患者更为明显。这种与葡萄糖不耐受成比例的对口服葡萄糖负荷的GIP反应过度表明糖尿病患者β细胞对GIP的反应相对失败，且糖尿病患者中GIP分泌过多所涉及的机制是胰岛素对GIP释放的抑制作用减弱。
