Diet Glycemic Load & Metabolism in Obese Pregnant Women
Diet Glycemic Load & Metabolism in Obese Pregnant Women
批准号:
6923313
负责人:
JANET C KING
金额:
$35.95万
依托单位国家:
美国
项目类别:
财政年份:
2005
资助国家:
美国
项目状态:
已结题
起止时间:
2005-09-20 至 2010-05-31
关键词:
body compositioncarbohydrate metabolismclinical researchdiabetes riskdiet therapydietary carbohydratesgestational diabetes mellitusglucose tolerance testhormone regulation /control mechanismhuman pregnant subjecthuman therapy evaluationinsulininsulin sensitivity /resistancelipid metabolismlipolysisliver metabolismmother /embryo /fetus nutritionnutrition related tagobesitypatient oriented research
中文摘要
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易发生代谢异常(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肥胖和2型糖尿病在以后的生活。低血糖负荷饮食可降低非妊娠妇女的血糖和胰岛素反应
成年人了我们假设,低血糖负荷(GL)饮食消耗在后半期,
怀孕降低了胰岛素、葡萄糖、游离脂肪酸对膳食的反应,这反过来又减少了肥胖孕妇,特别是内脏脂肪增加的孕妇的GDM和胎儿过度生长。具体目的是:1)确定低GL饮食对110名肥胖者胰岛素、碳水化合物和脂肪代谢的影响,(>35%脂肪)妇女按内脏脂肪厚度分层,并从妊娠20周开始随机分配至低或中高GL饮食,并持续至足月; 2)评估低GL饮食对参与调节燃料代谢的空腹和餐后激素水平的影响(人绒毛膜生长催乳素、孕酮、瘦素、脂联素、催乳素、胰高血糖素、皮质醇、儿茶酚胺和胃饥饿素);和3)确定妊娠后半期摄入低GL饮食是否降低GDM和巨大儿的患病率。在第28周和第34周,将测量激素和底物对标准100 g口服葡萄糖耐量试验和标准化低或中高GL餐的反应;还将在第34周胰岛素抵抗达到峰值时测量肝葡萄糖生成和脂解
在怀孕期间我们的研究结果可能为降低肥胖孕妇妊娠期糖尿病和巨大儿的风险提供一种新的饮食策略。此外,还将产生关于母亲碳水化合物摄入来源如何影响妊娠期碳水化合物和脂质代谢的新信息。
英文摘要
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.
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