Longitudinal studies of the rhesus monkey reveal a syndrome of diabetes mellitus in those that become middle-aged and obese. The sequence of events in the development of the disease progresses from normoinsulinemia with normoglycemia through stages of hyperinsulinemia followed by below normal insulin levels with hyperglycemia and glycosuria. We believe the rhesus to be an excellent nonhuman primate model for maturity-onset diabetes in humans.

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In monkeys (Macaca mulatta) without hypothalamic lesions, food intake was found to increase with increasing age and body weight; however, food intake per kilogram body weight showed a decline over the same period of time. As the animals became older, the amount of food intake converted to body weight decreased dramatically (feeding efficiency). Water intake was shown to be closely coupled to food intake. Both daily food and water-intake data were highly reliable over a period of years. Monkeys with ventromedial hypothalamic lesions exhibited hyperphagia and increased feeding-efficiency ratios and eventual obesity. The obese animals developed symptoms of diabetes mellitus. Animals with lesions restricted primarily to the arcuate nucleus showed no hyperphagia but increased feeding efficiency. These animals exhibited decreased growth hormone release and a transitory elevation of serum insulin.