Kuhl C, Holst J J
Diabetes. 1976 Jan;25(1):16-23. doi: 10.2337/diab.25.1.16.
The influence of pregnancy on serum glucose, serum insulin, and plasma glucagon concentrations was studied in eight normal women and 14 nonobese gestational diabetics. Each normal individual was subjected to an oral glucose tolerance test in midpregnancy, and all subjects were investigated late in pregnancy and again four to six weeks postpartum. As compared with the postpartum values, fasting glucose concentration decreased during gestation in the normals and increased in the gestational diabetics, but the changes were small and insignificant. In contrast, fasting insulin concentration increased equally and significantly in pregnancy in both groups. Likewise, the glucagon concentration was enhanced in the fasting state in both groups in pregnancy. However, the molar insulin-to-glucagon ratio was significantly elevated in both normals and gestational diabetics. In late pregnancy the magnitude of the insulin response to oral glucose (i.e., the incremental insulin area above fasting baseline) was equally and significantly enhanced in the normals and the gestational diabetics. However, when the insulin response during the first 60 minutes of the OGTT was expressed per unit of glucose stimulus (i.e., the delta insulin/delta glucose ratio) a significantly higher mean response was found in the normal pregnants than in the gestational diabetics. In pregnancy and postpartum, plasma glucagon always decreased to levels significantly below fasting levels after glucose ingestion. In normal midpregnancy the degree of suppression of glucagon was close to that of postpartum, whereas an exaggerated and prolonged suppression was found in late pregnancy in the normals as well as the gestational diabetics. These findings indicate that plasma glucagon and serum insulin concentrations are profoundly influenced by pregnancy. As the changes, however, lead to an increased insulin-to-glucagon ratio, the diabetogenicity of pregnancy is not explained by this relationship.
在8名正常女性和14名非肥胖型妊娠糖尿病患者中研究了妊娠对血清葡萄糖、血清胰岛素和血浆胰高血糖素浓度的影响。每位正常个体在妊娠中期接受口服葡萄糖耐量试验，所有受试者在妊娠晚期以及产后4至6周再次接受检查。与产后值相比，正常孕妇在妊娠期空腹血糖浓度降低，而妊娠糖尿病患者则升高，但变化较小且无统计学意义。相比之下，两组孕妇在妊娠期空腹胰岛素浓度均显著升高。同样，两组孕妇在空腹状态下血浆胰高血糖素浓度在妊娠期均升高。然而，正常孕妇和妊娠糖尿病患者的胰岛素与胰高血糖素摩尔比均显著升高。在妊娠晚期，正常孕妇和妊娠糖尿病患者对口服葡萄糖的胰岛素反应幅度（即高于空腹基线的胰岛素增量面积）均显著增强。然而，当口服葡萄糖耐量试验前60分钟内的胰岛素反应以每单位葡萄糖刺激来表示（即胰岛素变化量/葡萄糖变化量比值）时，发现正常孕妇的平均反应显著高于妊娠糖尿病患者。在妊娠期间及产后，口服葡萄糖后血浆胰高血糖素总是降至显著低于空腹水平。在正常妊娠中期，胰高血糖素的抑制程度与产后相近，而在正常孕妇和妊娠糖尿病患者的妊娠晚期均发现了过度且持久的抑制。这些发现表明血浆胰高血糖素和血清胰岛素浓度受妊娠的影响很大。然而，由于这些变化导致胰岛素与胰高血糖素比值升高，妊娠的致糖尿病性无法用这种关系来解释。
