CD36 is an 88-kDa membranous protein with multiple relevant function that is widely expressed in human tissues (1). Because we and others (2) found human genetic deficiency of this molecule, we have elucidated the molecular bases and pathophysiology. We have reported that the human deficiency may be associated with insulin resistance (3) and abnormal dynamics of long-chain fatty acid (LCFA)(4). The aim of the present study was to further characterize lipid and lipoprotein metabolism in the human genetic CD36 deficiency, especially focusing on postprandial responses.

Seven Japanese patients with type I CD36 deficiency (cases 1-7) were subjected. They were divided into the following two groups: group A, two younger patients we have recently identified (cases 1 and 2); and group B, patients> 50 years of age (cases 3-7, reported in our previous paper f3]). For the analysis of each group, aged-matched healthy and nonobese volunteers were subjected as control subjects (Table 1). First, we confirmed that insulin resistance was also present in the two younger patients (group A).