Nakanome C, Akai H, Umezu M, Toyota T, Goto Y, Furukawa Y, Sato T, Yumita S, Bloom S R
Nihon Naibunpi Gakkai Zasshi. 1982 Feb 20;58(2):98-109. doi: 10.1507/endocrine1927.58.2_98.
Plasma gastric inhibitory polypeptide (GIP), insulin, glucagon concentrations and blood glucose levels in response to the ingestion of 100 g glucose were measured in 5 patients with hyperparathyroidism in order to elucidate the effect of hypercalcemia on the release of these hormones. In addition, the effect of acute hypercalcemia on the release of these hormones in response to glucose ingestion was investigated in normal subjects. Fasting plasma GIP concentration in patients with hyperparathyroidism was significantly greater than the value in seventeen normal subjects. Significantly higher responses of plasma GIP and insulin were observed after the glucose ingestion in the patients with hyperparathyroidism as compared with the values in the normal subjects, and integrated GIP and insulin responses to the glucose ingestion for 120 min in the patients with hyperparathyroidism were significantly greater than the values in the normal subjects. On the other hand, plasma glucagon concentration after the glucose ingestion in the patients with hyperparathyroidism remained unchanged, although plasma glucagon concentrations after the glucose ingestion decreased significantly from the basal value in the normal subjects. Blood glucose levels after the glucose ingestion in two groups increased significantly from the basal value in the same manner. In nine normal subjects calcium infusion (4 mg/kg bolus injection followed by continuous infusion of 4 mg/kg/hr for 3 hr) caused a significantly high concentration of plasma calcium (11.5 approximately 13.0 mg/dl) from the basal value. Significantly higher responses of plasma GIP and insulin to the glucose ingestion were observed during calcium infusion as compared with the values during saline infusion. On the other hand, plasma glucagon concentration after the glucose ingestion was not significantly changed during calcium infusion in contrast with a significant decrease of plasma glucagon after the glucose ingestion during saline infusion. Consequently, calcium was considered to play a major part in the release of GIP and insulin. The characteristic response of plasma glucagon during calcium infusion was considered, at least in part, to protect the hypoglycemia caused by hyperinsulinemia.
为了阐明高钙血症对这些激素释放的影响，对5例甲状旁腺功能亢进患者摄入100克葡萄糖后的血浆胃抑制多肽（GIP）、胰岛素、胰高血糖素浓度及血糖水平进行了测定。此外，还研究了正常受试者急性高钙血症对葡萄糖摄入后这些激素释放的影响。甲状旁腺功能亢进患者的空腹血浆GIP浓度显著高于17名正常受试者的值。与正常受试者相比，甲状旁腺功能亢进患者摄入葡萄糖后血浆GIP和胰岛素的反应明显更高，甲状旁腺功能亢进患者对葡萄糖摄入120分钟的GIP和胰岛素综合反应明显高于正常受试者的值。另一方面，甲状旁腺功能亢进患者摄入葡萄糖后的血浆胰高血糖素浓度保持不变，而正常受试者摄入葡萄糖后的血浆胰高血糖素浓度从基础值显著下降。两组摄入葡萄糖后的血糖水平均以相同方式从基础值显著升高。在9名正常受试者中，静脉输注钙（先静脉推注4mg/kg，然后以4mg/kg/小时的速度持续输注3小时）使血浆钙浓度从基础值显著升高（11.5至约13.0mg/dl）。与输注生理盐水期间的值相比，在输注钙期间观察到血浆GIP和胰岛素对葡萄糖摄入的反应明显更高。另一方面，与输注生理盐水期间葡萄糖摄入后血浆胰高血糖素显著下降相反，输注钙期间葡萄糖摄入后血浆胰高血糖素浓度没有显著变化。因此，钙被认为在GIP和胰岛素的释放中起主要作用。输注钙期间血浆胰高血糖素的特征性反应至少部分被认为是为了保护由高胰岛素血症引起的低血糖。
