EFFECTS OF DIET DIFFERING IN GLYCEMIC INDEX

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. There is increasing evidence that insulin resistance, chronic subclinical inflammation, and Thrombosis/impaired fibrinolysis play a role in the development and progression of coronary heart disease (CHD) and type 2 diabetes mellitus. These processes are particularly accelerated in overweight/obese individuals. Although insulin resistance, hyperinsulinemia, and some markers of inflammation and thrombosis/impaired fibrinolysis are greater among African Americans (AA) compared to Caucasians (C), the possibility that these factors are related to greater disease prevalence in AA is unknown. Early intervention aimed at the reduction of these processes may be crucial for disease risk reduction. Diets differing in glycemic index (GI) and glycemic load (GL), referring to the glycemic responses induced by foods and the accompanying insulin secretion, could be beneficial in this context, because they may have an effect on circulating insulin and/or improve insulin sensitivity (Si). There is a lack of randomized, controlled trial evaluating the effects of dietary interventions differing in GI and GL on insulin resistance. inflammation, and thrombosis/fibrinolysis. Therefore, we propose to conduct a randomized, cross-over controlled feeding study of low- and high-GI/GL diets (4 weeks each) in 25 overweight or obese AA and C men to investigate these effects. The objectives of this study are 1) to compare the effects of matched diets differing only in GI and GL in overweight/obese men on insulin sensitivity (Si), markers of inflammation, and markers of thrombosis and fibrinolysis; 2) to assess whether the responses to low- and high- GVGL dietary interventions are predicted by baseline insulin concentration and/or Si; 3) to assess the effects of the low-and high-GI/GL dietary interventions on satiety. The study design includes 1) conducting a randomized, cross-over controlled feeding study of low- and high-GI/GL diets (4 weeks each) in 25 overweight/ obese AA and C men; 2) measuring baseline and post-intervention fasting serum concentrations of insulin and glucose. and comparing these in low- and high-GI/GL diets; 3) measuring baseline and post-intervention Si and the acute insulin response to glucose (AIRg), and comparing these in low- and high-GI/GL diets; 4) and measuring baseline and postintervention satiety scores, and comparing these in the low- and high-GI/GL diets. We hypothesize that 1) a low-GI/GL diet will result in lower fasting insulin and AIRg and higher Si relative to the high-GI/GL diet; 2) a low-GI/GL diet will result in lower plasma concentrations of markers of inflammation relative to the high-GI/GL diet; 3) a low GI/GL diet will result in lower plasma concentrations of PAI-1 and fibrinogen relative to the high-GI/GL diet; 4) the low-GI/GL diet will be greater in subjects with higher baseline insulin concentrations and/or lower Si, primarily AA; 5) and the low-GI/GL diet will result in greater satietv than the high-GI/GL diet.