EXERCISE AND A HIGH CARBOHYDRATE DIET: EFFECTS ON INSULIN ACTION

点击翻译按钮获取中文摘要

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.