Diet Glycemic Load & Metabolism in Obese Pregnant Women

描述(申请人提供)：三分之一的孕妇肥胖。肥胖孕妇比非肥胖孕妇更容易出现代谢异常(胰岛素抵抗、高血糖和高脂血症)和妊娠期糖尿病(GDM)。他们也有更大的婴儿，更容易在以后的生活中患肥胖症和2型糖尿病。低血糖负荷饮食可降低非妊娠患者的血糖和胰岛素对膳食的反应 成年人。我们假设低血糖负荷(GL)饮食在 怀孕会降低胰岛素、葡萄糖、游离脂肪酸对膳食的反应，进而减少肥胖孕妇的妊娠期糖尿病和胎儿过度生长，特别是那些内脏脂肪增加的孕妇。研究的具体目标是：1)确定低GL饮食对110名肥胖(&gt；35%脂肪)妇女胰岛素、碳水化合物和脂肪代谢的影响；按内脏脂肪厚度分层，从妊娠20周开始并持续到足月，随机分配到低或中高GL饮食；2)评估低GL饮食对与调节燃料代谢有关的空腹和餐后激素水平的影响(绒毛膜促生长激素、孕酮、瘦素、脂联素、催乳素、胰升糖素、皮质醇、儿茶酚胺和Ghrelin)；以及3)确定在怀孕后一半时间摄入低GL饮食是否降低了妊娠期糖尿病和胎儿巨大症的患病率。在28周和34周时，荷尔蒙和底物的反应将被测量到标准的100克口服葡萄糖耐量试验和标准化的低或中高甘油三酯膳食；当胰岛素抵抗达到顶峰时，也将在34周时测量肝脏葡萄糖产生和脂肪分解。 在怀孕期间。我们的研究结果可能为降低肥胖孕妇患妊娠期糖尿病和巨大儿的风险提供新的饮食策略。此外，还将产生关于母亲碳水化合物摄入来源如何影响怀孕期间碳水化合物和脂肪代谢的新信息。

DESCRIPTION (provided by applicant):One-third of all pregnant women are obese. Obese pregnant women develop metabolic abnormalities (insulin resistance, hyperglycemia, and hyperlipidemia), and gestational diabetes mellitus (GDM) more frequently than do non-obese women. They also have larger babies more prone to obesity and type 2 diabetes later in life. Low glycemic load diets lower the glycemic and insulin response to meals in nonpregnant adults. We hypothesize that a low glycemic load (GL) diet consumed during the last half of pregnancy lowers the insulin, glucose, free fatty acid response to meals which, in turn, reduces GDM and fetal overgrowth in obese pregnant women, especially those with increased visceral fat. The specific aims are 1) to determine the effects of a low GL diet on insulin, carbohydrate, and fat metabolism in 110 obese (>35% fat) women stratified by visceral fat thickness and randomly assigned to a low or moderately-high GL diet beginning at 20 weeks gestation and continuing to term; 2) to evaluate the effects of low GL diets on the levels of fasting and postprandial hormones involved in regulating fuel metabolism (human chorionic somatomammotropin, progesterone, leptin, adiponectin, prolactin, glucagon, cortisol, catecholamines, and ghrelin); and 3) to determine if consuming low GL diets the last half of pregnancy reduces the prevalence of GDM and fetal macrosomia. At 28 and 34 weeks, the hormonal and substrate response will be measured to a standard 100 g oral glucose tolerance test and to standardized low or moderately-high GL meals; hepatic glucose production and lipolysis will also be measured at 34 weeks when insulin resistance reaches its peak during gestation. The results of our study may provide a new dietary strategy for reducing the risk of gestational diabetes and fetal macrosomia in obese, pregnant women. In addition, new information on how the source of maternal carbohydrate intake affects carbohydrate and lipid metabolism in pregnancy will be generated.