EXERCISE AND A HIGH CARBOHYDRATE DIET: EFFECTS ON INSULIN ACTION

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。本方案研究高复合碳水化合物（HiCHO）饮食和运动对身体成分、胰岛素作用和肌肉代谢的影响。我们关于HiCHO饮食会导致体重减轻和胰岛素作用改善的假设是正确的。在一组糖耐量受损的老年受试者中，我们发现，随意摄入60% CHO、20%脂肪、20%蛋白质、25克纤维/1000千卡饮食的受试者不会减少能量摄入，但会减轻体重。这些数据表明，在不改变总能量摄入的情况下，减少脂肪摄入量可以达到负脂肪平衡。虽然这些数据具有挑衅性，但它们并没有直接解决通过减少脂肪摄入获得负脂肪平衡的假设。我们建议进一步验证这一假设，即通过改变膳食碳水化合物的组成来减少脂肪的摄入，从而达到负脂肪平衡。在我们之前的研究中我们看到超重的受试者食用高碳水化合物和高纤维的食物。即使体重减轻的受试者的计算能量摄入量没有减少，但由于膳食纤维摄入量的增加，实际可用能量可能减少了。我们建议使用相同的研究设计，为糖耐量受损的超重受试者提供具有相同宏量营养素组成（60% CHO， 20%脂肪和20%蛋白质）的饮食，但用血糖指数较高的简单碳水化合物代替复杂碳水化合物。我们将通过测量肝脏和脂肪细胞的新生脂肪生成和脂质氧化率来量化脂肪平衡。通过这种方式，我们将确定高血糖指数CHO导致脂质合成增加的程度，或者，正如我们假设的那样，即使在适应高CHO饮食后，重新生成脂肪的能力也非常有限。我们还将研究对脂质摄入量变化的反应。很多人推测，富含单不饱和脂肪和多不饱和脂肪的饮食有助于改善胰岛素的作用和更有利的体重。我们将给受试者提供富含多元和单一不饱和脂肪（40%脂肪、40% CHO和20%蛋白质）的随意饮食，以及具有相同常量营养素含量但饱和脂肪含量高的饮食（与阿肯色州中部的习惯饮食摄入量非常相似）。除了脂肪生成速率，我们还将在室内量热计中检查能量和底物平衡（摄入vs氧化）。将在饮食干预前后检查胰岛素刺激的葡萄糖处置。这些前瞻性，随机，对照试验将解决在2型糖尿病高风险受试者中改变宏量营养素摄入量的代谢后果这一重要问题。

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. This protocol investigates the effects of a high complex carbohydrate (HiCHO) diet and exercise on body composition, insulin action, and muscle metabolism. Our hypothesis that a HiCHO diet would result in weight loss and improved insulin action is correct. In a group of older subjects with impaired glucose tolerance, we showed that subjects who consume a 60% CHO, 20% fat, 20% protein, 25 g fiber/1000 kcal diet ad libitum do not decrease energy intake but decrease body weight. These data indicate that negative fat balance may be achieved by decreasing fat intake with no change in total energy intake. While these data are provocative, they do not directly address the hypothesis that negative fat balance is obtained by decreasing fat intake. We propose to further test the hypothesis that negative fat balance may be obtained through decreased fat intake by changing the composition of dietary carbohydrate. The results of our previous study we seen in overweight subjects consuming a diet high in complex carbohydrate and fiber. Even though calculated energy intake was not reduced in subjects who lost weight, actual available energy may have been reduced due to the increase dietary fiber intake. We propose to use the same study design and provide overweight subjects with impaired glucose tolerance a diet that has the same macronutrient composition (60% CHO, 20% fat, and 20% protein) but substitute simple carbohydrates with a higher glycemic index for complex carbohydrate. We will quantify fat balance by measuring both hepatic and adipocyte de novo lipogenesis and the rate of lipid oxidation. In this way we will determine the extent to which high glycemic index CHO results in increase lipid synthesis or, as we hypothesis, the capacity for de novo lipogenesis is very limited, even after adaptation to a high CHO diet. We will also examine the response to a change in lipid intake. There has been much speculation that a diet that is rich in mono and polyunsaturated fats contributes to improved insulin action and a more favorable body weight. We will feed subjects an ad libitum diet rich in poly and mono unsaturated fat (40% fat, 40% CHO, and 20% protein as well as a diet with the same macronutrient content but high in saturated fat (very similar to habitual dietary intake in Central Arkansas). In addition to rates of lipogenesis, we will also examine energy and substrate balance (intake vs oxidation) in our room calorimeter. Insulin stimulated glucose disposal will be examined before and after the dietary interventions. These prospective, randomized, controlled trials will address the important issue of the metabolic consequences of changing macronutrient intake in subjects at great risk for the development of type 2 diabetes.