Hasegawa H, Shirohara H, Okabayashi Y, Nakamura T, Fujii M, Koide M, Otsuki M
Second Department of Internal Medicine, Kobe University School of Medicine, Japan.
Metabolism. 1996 Feb;45(2):196-202. doi: 10.1016/s0026-0495(96)90053-0.
The role of glucose in the regulation of plasma cholecystokinin (CCK) level was investigated in healthy control subjects and patients with non-insulin-dependent diabetes mellitus (NIDDM). Plasma CCK concentration was determined by a specific and sensitive bioassay and by a highly sensitive and reliable double-antibody radioimmunoassay using OAL-656 as an antiserum. In control subjects, ingestion of Trelan G-75 (1,200 mOsm/L,225 mL), which is equivalent to 75 g glucose as metabolic products, caused a rapid and significant increase in plasma CCK bioactivity from 1.3 +/- 0.2 to a peak of 5.8 +/- 0.6 pmol/L and immunoreactive CCK concentration from 1.2 +/- 0.1 to 4.6 +/- 0.6 pmol/L. Ingestion of 75 g glucose in 225 mL water (33.3% solution) increased plasma CCK bioactivity to a similar degree to that observed following Trelan G-75 (peak response, 4.5 +/- 0.4 pmol/L). The same volume of 0.9% NaCl solution or water failed to increase plasma CCK concentration. A smaller dose of glucose (50 b/150 mL water) increased plasma CCK concentration, although the peak level (3.0 +/- 0.5 pmol/L) was less than that observed following 75 g glucose. In patients with NIDDM, Trelan G-75 ingestion increased CCK concentration, but the peak level was lower, albeit insignificantly, than that of normal subjects. When the maximal increment of plasma CCK above the basal value was compared between control and NIDDM subjects, the differences were statistically significant (NIDDM, 3.6 +/- 0.1 pmol/L; control, 5.0 +/- 0.4; P < .01). However, integrated CCK responses to Trelan G-75 in NIDDM (165.8 +/- 15.5 pmol/120 min) were not significantly different from those in control subjects (189.8 +/- 15.9 pmol/120 min). Peak CCK bioactivity occurred within 10 to 30 minutes of ingestion, preceding the increase in glucose and insulin. These results suggest a possible effect of CCK on insulin release in humans, and that the CCK secretory response to glucose in well-controlled diabetic patients is not significantly altered.
在健康对照受试者和非胰岛素依赖型糖尿病（NIDDM）患者中研究了葡萄糖在调节血浆胆囊收缩素（CCK）水平中的作用。采用特异性和灵敏的生物测定法以及使用OAL-656作为抗血清的高灵敏且可靠的双抗体放射免疫测定法测定血浆CCK浓度。在对照受试者中，摄入相当于75g葡萄糖代谢产物的Trelan G-75（1200mOsm/L，225mL）导致血浆CCK生物活性从1.3±0.2迅速显著增加至峰值5.8±0.6pmol/L，免疫反应性CCK浓度从1.2±0.1增加至4.6±0.6pmol/L。摄入225mL水中的75g葡萄糖（33.3%溶液）使血浆CCK生物活性增加至与Trelan G-75摄入后观察到的相似程度（峰值反应，4.5±0.4pmol/L）。相同体积的0.9%氯化钠溶液或水未能增加血浆CCK浓度。较小剂量的葡萄糖（50g/150mL水）增加了血浆CCK浓度，尽管峰值水平（3.0±0.5pmol/L）低于75g葡萄糖摄入后的水平。在NIDDM患者中，摄入Trelan G-75增加了CCK浓度，但峰值水平低于正常受试者，尽管差异不显著。当比较对照和NIDDM受试者血浆CCK高于基础值的最大增量时，差异具有统计学意义（NIDDM，3.6±0.1pmol/L；对照，5.0±0.4；P<0.01）。然而，NIDDM患者对Trelan G-75的CCK综合反应（165.8±15.5pmol/120分钟）与对照受试者（189.8±15.9pmol/120分钟）无显著差异。CCK生物活性峰值在摄入后10至30分钟内出现，早于葡萄糖和胰岛素的增加。这些结果提示CCK对人类胰岛素释放可能有影响，且血糖控制良好的糖尿病患者对葡萄糖的CCK分泌反应未显著改变。
