The positive correlation between GDR and BMI in the type 1 diabetic group is worth noting. Although the mechanism is unclear, the correlation could be related to the degree of glycemic control in type 1 diabetes as optimal glucose control improves insulin sensitivity but may lead to weight gain. Unlike the variable glucose disposal rates among the three groups, a sharp decline in FAA concentration was universal during HEC in all three groups. Insulin is known to promote the synthesis of fatty acids in the liver and reduce the breakdown of fat in the adipose tissue by inhibiting hormone sensitive lipase activities. Despite the known fact that FAA are elevated in type 2 diabetes, the high insulin concentration used during HEC obliterated the differences in FAA but not glucose disposal among the three groups, raising the likely possibility that that regional insulin resistance towards glucose metabolism not fat metabolism, may underlie the pathophysiology of IR in AA. Using HEC, we have documented that A-FABP is closely associated with IR but mostly in the control group and not so tightly once diabetes has occurred. This supports that IR has a greater effect on FABP levels in non-diabetic controls than in the diabetic state and suggests that other factors besides IR regulates FABP once diabetes has developed. The strong correlation of A-FABP to IR, SCH772984 942183-80-4 independent of BMI, may have a clinical relevance to screening for risks of diabetes in AA because generalized obesity is not common and a blood test is simple for assessing IR. Furthermore, the existing correlation independent of BMI also suggests that A-FABP levels may not be regulated by pathways related to obesity. A-FABP, a cytoplasmic protein abundantly present in serum and expressed only in adipocytes and macrophages, avidly binds to intracellular fatty acids. Their functions include the transport of FFA to cytoplasmic compartments in addition to regulating gene expression relating to lipid metabolism and inflammatory cytokines. FABP has been shown to be regulated by glucocorticoids, PPAR-c agonists, fatty acids and insulin, which may provide the mechanic framework for the link to insulin sensitivity. In a longitudinal studies from Hong Kong, serum A-FABP was associated with glucose intolerance and predicted the development of type 2 diabetes in a Chinese cohort followed over ten years, pointing to its potential as a prognostic tool. Similarly, A-FABP was associated with metabolic syndrome independent of adiposity and IR, expanding its role as a predictor for cardiovascular diseases. However, our results, although limited by the small sample size, raises the hypothesis that diagnostics targeting A-FABP may only be effective before the onset of diabetes. In contrast to earlier studies, we did not find RBP-4 to be correlated to GDR. The original publication linking RBP-4 to IR was done in Caucasians only. Our study also differed from the conclusion of a study from China showing a correlation of RBP-4 to IR, in that we studied AA and used a different assay.