EXERCISE AND GLUCOSE HOMEOSTASIS IN GESTATIONAL DIABETES

妊娠期糖尿病(GDM)导致围产儿发病率和死亡率 部分原因是胎儿对母亲高血糖的高胰岛素反应。 导致母体高血糖的代谢缺陷(S)尚未被 最终确定，但可能包括胰岛素的两种异常 释放胰岛素，降低胰岛素敏感性。此外，目前的管理 妊娠期糖尿病需要对所有妊娠期糖尿病和胰岛素治疗进行昂贵的监测 50%的病例，但并不能消除胎儿巨大儿的风险， 手术分娩和新生儿发病率是这种疾病的特点。 体育锻炼增加胰岛素敏感性并改善血糖 对非妊娠NIDDM患者进行控制并提供潜在成本 减少妊娠期糖尿病相关发病率的有效工具。期间未进行任何研究 然而，怀孕研究人员研究了体育锻炼对 胰岛素的作用。我们计划扩大对急性和慢性疾病的研究 孕期锻炼以解决这些问题，并检查 体育锻炼对妊娠期糖尿病患者代谢控制的潜在影响。 首先，研究胰岛素释放异常在妊娠期糖尿病中的作用。 高血糖钳夹在一组患有(n=30)或 无妊娠期糖尿病史者12例。这些女性将被录取 怀孕前，以及怀孕对胰岛素释放和 敏感性，以及这些变化在GDM发病机制中的作用 接受检查。该队列中患有妊娠期糖尿病的受试者将被随机分配到 运动训练和非运动训练的6周试验，以及 这项关于早期胰岛素释放和敏感性的试验将 量化的。第二个方案将检查不同的 单项运动训练与外周慢性运动训练的比较 内源性葡萄糖产生的胰岛素敏感性和可抑制性 使用正血糖钳夹。第二项议定书的主题将包括 瘦(20)和肥胖(20)非糖尿病和妊娠期糖尿病(20) 孕妇随机参加为期6周的训练/久坐试验。 这些协议应该定义体育训练可以通过的机制 改善妊娠期糖尿病患者的血糖控制，并量化这种影响以评估 运动在控制这种疾病方面的治疗潜力。

Gestational diabetes (GDM) results in perinatal morbidity and mortality due, in part, to fetal hyperinsulemic response to maternal hyperglycemia. The metabolic defect(s) producing maternal hyperglycemia has not been conclusively identified, but may include both abnormalities in insulin release and reduced insulin sensitivity. Furthermore, present management of GDM requires costly surveillance of all GDM and insulin therapy in up to 50% of cases, yet does not eliminate the risks of fetal macrosomia, operative delivery and neonatal morbidity characteristic of this disorder. Physical exercise increases insulin sensitivity and improves glucose control in nonpregnant patients with NIDDM and offers a potentially cost effective tool for reducing GDM related morbidity. No studies during pregnancy, however, have examined the effect of physical training on insulin action. We plan to extend our studies of the acute and chronic exercise during pregnancy to resolve these questions and to examine the potential impact of physical exercise on metabolic control in GDM. First, the role of abnormal insulin release in GDM will be examined by use of the hyperglycemic clamp in a cohort of parous subjects with (n=30) or without (n=12) prior gestational diabetes. These women will be enrolled prior to conception, and the effect of pregnancy on insulin release and sensitivity, and the role of these changes in the pathogenesis of GDM will be examined. Subjects in this cohort who develop GDM will be randomized to a 6 week trial of exercise training and non-exercise, and the effect of this trial on early phase insulin release and sensitivity will be quantified. A second protocol will examine the differential effects of an isolated exercise session versus chronic exercise training on peripheral insulin sensitivity and supressability of endogenous glucose production using the euglycemic clamp. Subjects for the second protocol will include lean (20) and obese (20) non-diabetic and gestational diabetic (20) pregnant women who will be randomize to a 6 week training/sedentary trial. These protocols should define the mechanism by which physical training may improve glycemic control in GDM, and quantify this effect to evaluate the therapeutic potential of exercise in managing this disorder.