This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.The prevalences of diabetes and obesity are rising in parallel to epidemic proportions. One of the links between these two conditions is insulin resistance with obesity being one of the primary causes of insulin resistance and insulin resistance being one of the pathphysiological hallmarks of type 2 diabetes. Overnutrition is felt to be one of the primary reasons that obesity has become so prevalent in our society. This proposal seeks to elucidate the mechanism whereby excess energy intake results in insulin resistance. We hypothesize that an overfeeding will result in an imbalance in the subunits of one of the insulin signaling proteins in skeletal muscle. This imbalance in these subunits will be the primary mechanism resulting in insulin resistance at a whole body level. To explore this hypothesis we will overfeed healthy volunteers for 5 days on either a low-fat or a high-fat diet and measure the changes in whole body and muscle insulin action as compared to 'normal' feeding.
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