Defects in oxidative and nonoxidative glucose metabolism may be involved in the insulin resistance of aging, possibly linked to a central redistribution of body fat. By hyperinsulinemic-euglycemic clamps with whole-body indirect calorimetry, we assessed the contributions of oxidative and nonoxidative glucose disposal to insulin action in 12 elderly persons and 2 groups of younger subjects (14 in each) who had participated in a large population study. Subjects from Young-1 were individually matched to the elderly persons by body mass index and had similar waist circumferences, whereas subjects from Young-2 had a body mass index typical of their age group in the population study and smaller waist measurements. In the combined sample, we also considered possible determinants, related to age and central fat, of flux through these metabolic pathways. The elderly persons had lower nonoxidative glucose disposal compared with the men in Young-2 ( P = .0450 by analysis of variance), whereas glucose oxidation did not differ between the groups. Glucose oxidation correlated negatively with waist circumferences, triglycerides, and alanine aminotransferase and positively with total testosterone and sex hormone-binding globulin. Nonoxidative glucose metabolism correlated inversely with waist circumferences, triglycerides, and free fatty acids and positively with maximum O 2 consumption and total testosterone. In the best regression models, alanine aminotransferase and triglycerides were negatively associated with glucose oxidation (model R 2 = 39%), whereas lower baseline free fatty acids and higher maximum O 2 consumption and sex hormone-binding globulin predicted enhanced nonoxidative glucose metabolism (model R 2 = 47%). These results substantiate that measures to avert abdominal adiposity may prevent insulin resistance and its related metabolic derangements in elderly persons.