Dornhorst A, Bailey P C, Anyaoku V, Elkeles R S, Johnston D G, Beard R W
Department of Clinical Endocrinology, Imperial College of Science, Technology and Medicine, St Mary's Hospital Medical School, London.
Q J Med. 1990 Dec;77(284):1219-28. doi: 10.1093/qjmed/77.3.1219.
Glucose tolerance and insulin secretion were studied in 56 women 6-12 years following a pregnancy complicated by gestational diabetes, and in 23 matched controls. At recall 14 women were known to have diabetes and five were again pregnant with recurrent gestational diabetes. The early development of diabetes was associated with a fasting plasma glucose greater than 6 mmol/l during pregnancy and with a high plasma glucose response to oral glucose which persisted after delivery. Obesity was predictive of non-insulin-dependent diabetes whereas those that later required insulin were not obese. At recall, seven of the remaining 37 women were found to have unrecognized diabetes, 13 had impaired glucose tolerance (IGT) and 17 were normal by WHO criteria using a 75 g oral glucose tolerance test. In these 37 women, fasting plasma glucose and the glucose response to oral glucose in pregnancy were not predictive of subsequent diabetes or impaired glucose tolerance. Obesity in pregnancy and subsequent weight gain were associated with non-insulin-dependent diabetes and impaired glucose tolerance at recall. Insulin deficiency was observed during the oral glucose tolerance test in the diabetics (the mean +/- SEM ratio insulin area:glucose area 4.1 +/- 1.3 diabetics, 10.7 +/- 1.8 controls, p less than 0.05), whereas in the group with impaired glucose tolerance insulin levels were high and in proportion to their hyperglycaemia (insulin area:glucose area 10.9 +/- 1.4 IGT, 9.4 +/- 1.4 controls). Women with normal glucose tolerance and previous gestational diabetes had significantly lower insulin responses than their controls, despite mild hyperglycaemia (insulin area:glucose area 4.0 +/- 0.7 normal glucose tolerance, 7.6 +/- 1.1 controls, p less than 0.02). Abnormalities of glucose tolerance and insulin secretion are present following a gestational diabetic pregnancy. Gestational diabetes identifies women at risk for developing diabetes and impaired glucose tolerance, both of which are risk factors for premature vascular disease.
对56名妊娠合并妊娠期糖尿病的女性在产后6至12年进行了葡萄糖耐量和胰岛素分泌研究，并与23名匹配的对照组进行了比较。在随访时，已知14名女性患有糖尿病，5名再次妊娠并发复发性妊娠期糖尿病。糖尿病的早期发展与孕期空腹血糖大于6 mmol/l以及产后持续存在的口服葡萄糖后高血糖反应有关。肥胖是非胰岛素依赖型糖尿病的预测因素，而后来需要胰岛素治疗的患者并不肥胖。在随访时，其余37名女性中有7名被发现患有未被识别的糖尿病，13名葡萄糖耐量受损（IGT），17名根据世界卫生组织标准使用75 g口服葡萄糖耐量试验结果正常。在这37名女性中，孕期空腹血糖和口服葡萄糖后的血糖反应并不能预测随后的糖尿病或葡萄糖耐量受损。孕期肥胖和随后的体重增加与随访时的非胰岛素依赖型糖尿病和葡萄糖耐量受损有关。在糖尿病患者的口服葡萄糖耐量试验中观察到胰岛素缺乏（糖尿病患者胰岛素面积与葡萄糖面积的平均±SEM比值为4.1±1.3，对照组为10.7±1.8，p<0.05），而在葡萄糖耐量受损组中胰岛素水平较高且与高血糖成比例（胰岛素面积与葡萄糖面积的比值为10.9±1.4 IGT，9.4±1.4对照组）。尽管有轻度高血糖，但葡萄糖耐量正常且既往有妊娠期糖尿病的女性的胰岛素反应明显低于对照组（胰岛素面积与葡萄糖面积的比值为4.0±0.7葡萄糖耐量正常，7.6±1.1对照组，p<0.02）。妊娠期糖尿病妊娠后存在葡萄糖耐量和胰岛素分泌异常。妊娠期糖尿病可识别出有患糖尿病和葡萄糖耐量受损风险的女性，而这两者都是过早发生血管疾病的危险因素。
