Resistance of glucose and fatty acid (FA) metabolism to the effects of insulin is an important feature on human type 2 diabetes. Susceptibility to these symptoms is in part genetic as demonstrated by studies of families and twins. Recent studies suggest that mutations in a gene coding for a membrane protein involved in cellular uptake of long-chain FA may underlie the predisposition to type 2 diabetes. Mutations in this gene would result in defective FA Levels. High FA induce insulin resistance by inhibiting insulin stimulation of glucose utilization via inhibition of uptake and phosphorylation of glucose. Thus, our hypothesis which is supported by work with an animal (rat) model of type 2 diabetes is that a primary defect in FA uptake, due to mutations in the CD36 gene, would underline the genetic predisposition to diabetes type 2 in humans. We propose to screen type 2 diabetics to determine if they exhibit a higher incidence of CD36 mutations than the general population. Defects in FA uptake will then be explored non-invasively by imaging of the heart muscle using scintigraphy and iodinated derivative.