DIMINISHED B-CELL SECRETORY CAPACITY IN PATIENTS WITH NONINSULIN-DEPENDENT DIABETES-MELLITUS
DIMINISHED B-CELL SECRETORY CAPACITY IN PATIENTS WITH NONINSULIN-DEPENDENT DIABETES-MELLITUS
复制标题
DOI：
10.1172/jci111542
复制
发表时间：
1984-01-01
影响因子：
15.9
通讯作者：
PORTE, D
中科院分区：
文献类型：
--
作者：
WARD, WK;BOLGIANO, DC;PORTE, D
为了评价非胰岛素依赖型糖尿病（NIDDM）患者是否具有正常的胰岛素分泌能力，在8例未经治疗的NIDDM患者和8例非糖尿病对照者中测定了B细胞对葡萄糖增强效应的最大反应性。在5个匹配的血浆葡萄糖水平下测量对5g静脉内精氨酸的急性胰岛素反应，所述血浆葡萄糖水平范围为100-615 mg/dl。使用非线性回归拟合Michaelis-Menten方程的修改，估计急性胰岛素反应接近的上渐近线（AIRmax）和半最大反应时的血糖浓度（PG 50）。此外，在这些相同的葡萄糖水平下测量胰高血糖素对精氨酸的反应，以比较糖尿病患者和对照组中高血糖症对A细胞的最大抑制。在所有血糖水平下，糖尿病患者对精氨酸的胰岛素反应均低于对照组（P < 0.001）。此外，糖尿病患者的AIRmax估计值比对照组低得多（83 . ±. 21对450。93 μ U/ml，P < 0.01）。相比之下，PG 50在糖尿病患者和对照组中相似（234 . ±. 28对197 +-。20 mg/dl，P等于NS [不显著]），并且两组中的胰岛素应答在葡萄糖水平为0.0000000时接近或达到最大值。460毫克/分升。在所有血糖水平下，NIDDM患者对精氨酸的急性胰高血糖素反应均显著高于对照组。此外，尽管对照受试者中的胰高血糖素反应在葡萄糖水平为0.0000000时达到最小值。460 mg/dl时，糖尿病患者的反应在整个葡萄糖范围内持续下降，未达到最低值。因此，在NIDDM患者中，A线圈对葡萄糖水平变化的敏感性可能会降低。NIDDM患者对葡萄糖增强效应的最大胰岛素反应性明显降低。这种缺陷表明B细胞分泌能力降低，并提示NIDDM患者B细胞功能明显受损。
In order to assess whether patients with noninsulin-dependent diabetes mellitus (NIDDM) possess normal insulin secretory capacity, maximal B cell responsiveness to the potentiating effects of glucose was estimated in 8 untreated patients with NIDDM and in 8 nondiabetic controls. The acute insulin response to 5 g i.v. arginine was measured at 5 matched plasma glucose levels that ranged from .apprx. 100-615 mg/dl. The upper asymptote approached by acute insulin responses (AIRmax) and the plasma glucose concentration at half-maximal responsiveness (PG50) were estimated using nonlinear regression to fit a modification of the Michaelis-Menten equation. In addition, glucagon responses to arginine were measured at these same glucose levels to compare maximal A cell suppression by hyperglycemia in diabetics and controls. Insulin responses to arginine were lower in diabetics than in controls at all matched glucose levels (P < 0.001 at all levels). In addition, estimated AIRmax was much lower in diabetics than in controls (83 .+-. 21 vs. 450 .+-. 93 .mu.U/ml, P < 0.01). In contrast, PG50 was similar in diabetics and controls (234 .+-. 28 vs. 197 .+-. 20 mg/dl, P equals NS [not significant]) and insulin responses in both groups approached or attained maxima at a glucose level of .apprx. 460 mg/dl. Acute glucagon responses to arginine in patients with NIDDM were significantly higher than responses in controls at all glucose levels. In addition, although glucagon responses in control subjects reached a minimum at a glucose level of .apprx. 460 mg/dl, responses in diabetics declined continuously throughout the glucose range and did not reach a minimum. Thus, A coil sensitivity to changes in glucose level may be diminished in patients with NIDDM. Patients with NIDDM possess markedly decreased maximal insulin responsiveness to the potentiating effects of glucose. Such a defect indicates the presence of a reduced B cell secretory capacity and suggests a marked generalized impairment of B cell function in patients with NIDDM.