Elevated serum lipid levels and/or abnormal carbohydrate-insulin mechanisms have been observed with increasing frequency in obese persons ( 13). In addition, abnormalities in lipid/carbohydrate metabolism have also been demonstrated in atherosclerotic and atherosclerotic prone individuals (6,8,9,12, 14). Similar metabolic abnormalities have been produced in rats made obese by lesions of the hypothalamus ( 3 ) . In this paper we report the development of hyperbeta-and hyperprebeta-lipoproteinemia, decreased glucose tolerance and abnormal serum insulin levels in association with obesity in a subhuman primate.Methods. Subjects. Data are reported on 19 male and 2 female monkeys (Macaca mu-Zatta) obtained commercially. The animals were classified arbitrarily as obese if their body weights exceeded 15 kg. Two groups of obese animals were studied: in one obesity was obtained by placement of lesions in the hypothalamus; in the other, obesity occurred spontaneously when the animals reached "middle age" (12-14 years old). Brain lesions were aimed at the ventromedial area of the hypothalamus, using the procedures of Hamilton and Brobeck (5). When properly placed, these lesions were followed by hyperphagia and obesity. Two of the spontaneously obese animals developed overt diabetes. No insulin was given for treatment of hyperglycemia and glycosuria. Throughout the study all animals were housed in individual cages

Normoinsulinemic, hyperinsulinémie and diabetic monkeys were given access to a 10-percent solution of sucrose water ad libitum. During the period of sucrose intake for the normal animals, circulating insulin and triglyceride levels rose and fell concomitantly. Monkeys with hyperinsulinemia exhibited a fall in serum insulin values, and the diabetic animals showed an exaggerated lipid response and no change in insulin levels.

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