CORRELATION BETWEEN MINIMAL SECRETORY CAPACITY OF PANCREATIC BETA-CELLS AND STABILITY OF DIABETIC CONTROL
CORRELATION BETWEEN MINIMAL SECRETORY CAPACITY OF PANCREATIC BETA-CELLS AND STABILITY OF DIABETIC CONTROL
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DOI：
10.2337/diabetes.37.1.81
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发表时间：
1988-01-01
期刊：
影响因子：
7.7
通讯作者：
SHIMA, K
中科院分区：
文献类型：
--
作者：
FUKUDA, M;TANAKA, A;SHIMA, K
胰腺β-淀粉样蛋白的最小分泌能力的意义对20例胰岛素依赖型糖尿病患者的血糖水平稳定性进行了研究。在这些患者中，还研究了低血糖反应中主要反调节激素的血浆浓度变化，以阐明其对糖尿病脆性的贡献。β-基于静脉内胰高血糖素试验期间血浆C肽免疫反应性（CPR）的升高，采用可检测低至0.03 ng/ml的血浆CPR的高灵敏度测定法评价细胞功能。在用胰高血糖素刺激后，在10名β-葡萄糖缺乏的患者中观察到血浆CPR的显著增加。通过传统的血浆CPR测定，细胞功能已被评估为完全耗尽。发现胰腺β-淀粉样蛋白的分泌能力与胰腺β-淀粉样蛋白的分泌能力之间存在明显的负相关。结果显示，用这种方法测量的细胞数与血糖不稳定程度呈负相关（r =-0.74，P <0.01）。以0.15 U. cntdot的速率输注胰岛素。kg-1. h ~（-1）持续60 min，血糖水平持续下降，导致10例CPR无应答者中7例出现神经性低血糖，而CPR应答者中仅2例出现神经性低血糖。在胰岛素诱导的低血糖期间，血浆胰高血糖素免疫反应性在CPR无应答者中没有增加，但在CPR应答者中显著增加。在最小残留β-γ之间发现了正相关。细胞容量和α-细胞与低血糖的相关性（r = .65，P < .01）。与他们的胰腺α-淀粉酶反应的差异相反，细胞对低血糖的反应，两组显示出或多或少相同的血浆肾上腺素、去甲肾上腺素、生长激素和皮质醇对低血糖的反应。胰岛素原储备的完全缺乏不可避免地导致循环胰岛素水平自动调节的丧失，并且似乎是引起糖尿病控制的高不稳定性的主要因素。缺乏. beta. -细胞功能可能与胰腺α-细胞功能障碍，这也部分导致脆性糖尿病的代谢变异性。
The significance of the minimal secretory capacity of pancreatic .beta.-cells for the stability of the plasma glucose level was studied in 20 patients with insulin-dependent diabetes mellitus. Changes in plasma concentrations of major counterregulatory hormones in response to hypoglycemia were also investigated in these patients to clarify their contribution to diabetic brittleness. .beta.-Cell function was evaluated on the basis of elevation of plasma C-peptide immunoreactivity (CPR) during the intravenous glucagon test with a highly sensitive assay for plasma CPR that could detect as little as 0.03 ng/ml. After stimulation with glucagon, a significant increase in plasma CPR was observed in 10 of the patients whose .beta.-cell function had been evaluated as completely depleted by a conventional assay for plasma CPR. A clear inverse correlation was found between the secretory capacity of pancreatic .beta.-cells measured in this way and the degree of glycemic instability (r = -.74, P < .01). Infusion of insulin at a rate of 0.15 U .cntdot. kg-1 .cntdot. h-1 for 60 min caused a continuous decrease in the plasma glucose level, resulting in neuroglycopenia in 7 of the 10 CPR nonresponders but only 2 of the CPR responders. During insulin-induced hypoglycemia, plasma glucagon immunoreactivity did not increase in the CPR nonresponders but increased significantly in the CPR responders. A positive correlation was found between the minimal residual .beta.-cell capacity and the responsiveness of .alpha.-cells to hypoglycemia (r = .65, P < .01). In contrast to the difference in the responses of their pancreatic .alpha.-cells to hypoglycemia, the two groups showed more or less the same responses of plasma epinephrine, norepinephrine, growth hormone, and cortisol to hypoglycemia. Total lack of insulinogenic reserve inevitably results in loss of automatic regulation of the circulating insulin level and seems to be a major factor in causing hyperlability of diabetic control. The lack of .beta.-cell function may be related causally to pancreatic .alpha.-cell dysfunction, which also contributes in part to metabolic variability in brittle diabetes.