Perley M J, Kipnis D M
J Clin Invest. 1967 Dec;46(12):1954-62. doi: 10.1172/JCI105685.
The plasma insulin responses of normal weight and obese, diabetic, and nondiabetic subjects to intravenous glucose was only 30-40% of that seen after oral glucose, indicating that alimentary mechanism(s) in addition to the arterial blood sugar concentration regulate insulin secretion. Observations made in subjects with diverted portal circulation indicate that the alimentary insulinogenic mechanism is located in the intestinal tract. The insulinogenic potency of the alimentary and glycemic stimuli expressed in terms of insulin secretion per gram of glucose were remarkably similar within each group of individuals. Between these groups, however, there were considerable differences. Obesity, with or without associated diabetes, was associated with a true hypersecretory responsiveness, whereas diabetes was characterized, with or without obesity, by a marked impairment in insulin secretion. The experimental design used in these studies permitted quantitation of the magnitude of the glycemic component of an oral glucose load. As a consequence of impaired insulin secretion, a greater than normal proportion of the oral glucose load escapes initial hepatic extraction in the maturity-onset diabetic and enters the peripheral circulation. Therefore, in the noninsulin-requiring maturity-onset diabetic, the glycemic insulinogenic stimulus for a given oral glucose load is significantly greater than in normal subjects and accounts for the excessive plasma insulin responses observed late in the course of an oral glucose tolerance test.
正常体重以及肥胖的糖尿病和非糖尿病受试者对静脉注射葡萄糖的血浆胰岛素反应仅为口服葡萄糖后反应的30%-40%，这表明除动脉血糖浓度外，消化机制也参与调节胰岛素分泌。对门静脉循环分流的受试者的观察表明，消化性胰岛素生成机制位于肠道。以每克葡萄糖分泌的胰岛素量来表示，消化刺激和血糖刺激的胰岛素生成能力在每组个体中非常相似。然而，这些组之间存在相当大的差异。无论是否伴有糖尿病，肥胖都与真正的高分泌反应性相关，而无论是否肥胖，糖尿病的特征都是胰岛素分泌明显受损。这些研究中使用的实验设计允许对口服葡萄糖负荷的血糖成分大小进行定量。由于胰岛素分泌受损，成年型糖尿病患者口服葡萄糖负荷中超过正常比例的部分在肝脏初次摄取时未被摄取，而是进入外周循环。因此，在非胰岛素依赖型成年型糖尿病患者中，给定口服葡萄糖负荷的血糖胰岛素生成刺激明显大于正常受试者，这解释了在口服葡萄糖耐量试验后期观察到的血浆胰岛素过度反应。
