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. Obesity has been increasing in prevalence the past generation and is a serious public health problem. Obesity is an important risk factor for cardiovascular disease, stroke, some types of cancer, and type 2 diabetes. Obesity leads to type 2 diabetes through insulin resistance. While there is strong evidence of a correlation between the decline in insulin sensitivity and the increase in body adipose tissue, the overall mechanistic association between body fat and insulin receptor sensitivity remains elusive. Regional fat distribution has been also considered as a modulating factor in the relationship between body fat and peripheral insulin action. A more recent consideration has been organ-specific fat accumulation, outside of the adipose tissue compartment. In particular, fatty acid accumulation in skeletal muscle may have a profound influence in whole-body insulin action measured by glucose uptake, since that tissue accounts for the largest proportion of insulin-responsive glucose utilization in the body. The proposed study will provide quantitative information on the contribution of intramyocellular lipid (IMCL) to insulin resistance associated with obesity. First, it will assess the effects of weight loss on the IMCL and insulin resistance of a group of healthy obese adults. Second, it will explore the correlation between insulin resistance and IMCL, BMI, total body fat (TBF), and serum triglyceride (TG) levels of the obese group with an otherwise similar group of lean individuals.
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