EFFECTS OF DIETARY MACRONUTRIENT INTAKE AND RESISTANCE TRAINING EXERCISE ON G

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 摘要 在过去的30年里，美国超重儿童（6-19岁）的患病率（BMV>第95百分位数）增加了3倍，2000年达到16%（NHANES）。 随着儿童超重的增加，儿童（0-19岁）2型糖尿病的发病率增加了4倍。 虽然肥胖相关的糖代谢损害的病因是多因素的，膳食大量营养素摄入和体力活动是潜在的重要因素。 该建议的目的是在健康青少年中确定1）肥胖对能量消耗和底物氧化、由糖原生成和糖原分解产生的葡萄糖、胰岛素分泌和敏感性以及脂解的影响; 2）12周的阻力训练运动计划是否会改善肥胖青少年的葡萄糖代谢，如果是，3）运动效果是否与总肌细胞内、内脏和/或肝脏脂肪含量的降低相关。 为了解决这些问题，12名超重（体脂>30%）和12名瘦（体脂<25%）的青少年将在两个场合进行研究（就在12周锻炼计划开始之前和最后一周锻炼结束时）;在所有受试者中，两个研究场合中的每一个都将在7天的高脂肪饮食之前进行。 将采用最先进的稳定同位素-GCMS技术和MRI来获得实现上述目标所需的数据。 这些研究提供的信息将提高我们对青少年肥胖代谢影响的理解，将导致识别可能增加，预防或延迟2型糖尿病发展的因素。 它也将帮助我们确定是否力量锻炼没有意图减肥将改善胰岛素敏感性和正常化的葡萄糖代谢超重青少年。 假设 总体假设：阻力训练运动（无减肥意图）改善胰岛素敏感性，正常化葡萄糖代谢，减少健康肥胖青少年的肌内脂肪，内脏脂肪和肝脏脂肪。 具体假设：H1。 一个12周的抗阻运动计划（x 2/周，1小时/次）增加肥胖青少年的胰岛素敏感性，但不是在已经胰岛素敏感的瘦青少年。 H2。 运动引起的胰岛素敏感性变化与运动引起的肌细胞内脂肪含量变化呈负相关。 H3. 12周的抗阻运动计划将通过减少肝脏脂肪堆积使肥胖青少年的肝脏再生正常化。 具体目标 确定12周的抗阻训练运动计划（x 2/周; 1小时/次）是否会增加肥胖青少年的胰岛素敏感性，减少胰岛素生成并降低肌细胞内和肝脏脂肪含量。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. ABSTRACT Over the past 30 y the prevalence of overweight children (6-19 y) in the USA (BMV>95th percentile) has increased 3-fold to reach 16% in 2000 (NHANES). Concomitant with the increase in childhood overweight, the incidence of type 2 diabetes in children (0-19 y) has increased 4-fold. Although the etiology of obesity related impairement of glucose metabolism is multifactorial, dietary macronutrient intake and physical activity are potentially important factors. The aims of this proposal are to determine in healthy adolescents 1) the impact of obesity on energy expenditure and substrate oxidation, glucose production from gluconeogenesis and glycogenolysis, insulin secretion and sensitivity, and lipolysis; 2) whether a 12 weeks resistance training exercise program will improve glucose metabolism in obese adolescents, and if so, 3) whether the exercise effect is correlated with a decrease in total intramyocellular, visceral and/or hepatic fat content. To address these questions, 12 over weight (body fat >30%) and 12 lean (body fat <25%) adolecents will be studied on two occasions (just prior to the start of a 12 weeks exercise program and at the end of the last week of exercise); in all subjects, each of the two study occasions will be preceded by 7-d of a high fat diet. State of the art stable isotope-GCMS techniques and MRI will be sued to obtain the data needed to address the aims stated above. The information provided by these studies will improve our understanding of the metabolic effects of obesity in adolescents, will lead to identifying factors which may increase, prvent or delay the development of type 2 diabetes. It will also help us determine whether strength exercise without intent to weight loss will improve insulin sensitivity and normalize glucose metabolism in over weight adolescents. HYPOTHESIS Overall hypotheses: Resistance training exercise (without intent of weight loss) improves insulin sensitivity, normalizes glucose metabolism and reduces intramyocellular, visceral and hepatic fat in healthy obese adolescents. Specific hypotheses: H1. A 12 weeks resistance exercise program (x 2/week, 1 h/session) increases insulin sensitivity in obese adolescents, but not in already insulin sensitive lean adolescents. H2. The exercise-induced changes in insulin snesitivity are inversely correlated with exercise-induced changes in intramyocellular fat content. H3. A 12 weeks resistance exercise program will normalize gluconeogenesis in obese adolescents by reducing hepatic fat accumulation. SPECIFIC AIMS To determine whether a 12 weeks resitance training exercise program (x 2/week; 1 h/session) would increase insulin sensitivity, reduce gluconeogenesis and decrease intramyocellular and hepatic fat content in obese adolescents.