High intakes of energy-dense diets by immature animals can result in a high growth rate that potentially induces obesity as these animals mature. Overfeeding during infancy apparently does not result in increased fat-cell numbers but rather promotes increased fat-cell size, particularly in female baboons (Lewis et al., 1989). Newborn baboons (Papio cynocephalus) were fed a commercial milk-replacer diet modified to contain ME at 40.5, 67.5, and 94.5 kcal per 100 g to produce underfed, normally fed, and overfed male and female infants at the age of 4 months. From the age of 4 months to 5 years, male and female baboons were fed a similar diet formulated to contain 40% of ME calories as lard, 39% as carbohydrate, and 21% as protein. Cholesterol was supplemented at 1.7 mg·kcal-1 of ME. At 5 years, females that had been overfed as infants had a significantly greater percentage of body mass that was fat, and mean fat cell volume was greater, when compared with females that were underfed or normally fed as infants. However, infant food intake did not significantly influence body composition or fat-cell number in 5-year-old male baboons. Nevertheless, in the context of the fat cell studies in baboons, it should be noted that obesity has not been described in this species. Such a fat-cell response in baboons might not be applicable to a species that develops spontaneous obesity, such as the rhesus monkey.
Reductions in fasting blood glucose resulting from diet restriction first became apparent in the Wisconsin rhesus macaques (M. mulatta) after 24 months (Kemnitz et al. 1994a), and in the NIH rhesus males after 36 months (Lane et al., 1995b). Differences in age at initiation of diet restriction, relative fractions of life span on diet restriction, severity of diet restriction, differences in body composition, and concentrations of sucrose in the diet were regarded as potential contributors to that discrepancy between studies (Lane et al., 1995b). It was noted, however, that differences in blood glucose concentration between ad libitum-fed and diet-restricted monkeys were observed in the Wisconsin monkeys shortly after the imposition of additional diet restriction 18 months into the study (Kemnitz et al., 1994a). After 8.5 years, a longitudinal study of semiannual glucose tolerance tests in the Wisconsin rhesus monkeys revealed that diet-restricted monkeys had increased insulin sensitivity, increased plasma glucose disappearance rate, reduced fasting plasma insulin concentration, and reduced insulin response to glucose compared to ad libitum-fed controls (Gresl et al., 2001). Chronic dietary restriction appeared to protect against development of insulin resistance in aging rhesus macaques and also might have improved glucoregulatory measures compared with those of otherwise normoinsulinemic monkeys.
Cefalu et al. (1997) reported that insulin sensitivity, as measured with frequent intravenous glucose-tolerance tests, was increased in purchased, feral adult cynomolgus macaques (M. fascicularis) after 1 year of diet restriction (target of 30% below ad libitum-fed, 34% actual). BW, total abdominal fat, and intra-abdominal fat, determined by computed tomographic scan, were all lower in diet-restricted than in ad libitum-fed cynomolgus monkeys. Those results demonstrate that diet restriction can ameliorate pathologic fat deposition; this change might be associated with a substantial improvement in peripheral-tissue insulin sensitivity.
Reductions in fasting blood glucose became apparent in NIH diet-restricted rhesus macaques (M. mulatta) after 3-4 years of restriction (Lane et al., 1995b). Maximal glucose concentrations, reached during intravenous glucose-tolerance tests, increased with age but were lower in diet-restricted monkeys than in ad libitum-fed controls. Several measures of the insulin response (baseline, maximum, and integrated areas under the curve) increased with age and were lower in diet-restricted monkeys. The age-related increase in maximal blood glucose concentration in ad libitum-fed monkeys, after intravenous glucose challenge, was probably related to decreased insulin sensitivity, inasmuch as insulin levels measured concurrently with glucose peaks during intravenous infusions were significantly increased among older, heavier animals. The age-related increase in the maximal glucose peak was inhibited in monkeys subjected to long-term diet restriction, and this difference between dietary treatments might be linked to increased insulin sensitivity in diet-restricted monkeys. Hansen and Bodkin (1993) reported that glucose disappearance rate was greater in diet-restricted rhesus monkeys than in ad libitum-fed controls, and insulin resistance was lower in diet-restricted, older rhesus (Bodkin et al., 1995). Those findings suggest that long-term diet restriction can be an effective means of mitigating the development of potentially pathologic insulin resistance in older rhesus monkeys.
Captive orangutans (Pongo spp.) have a propensity to become obese and develop diabetes (Gresl et al., 2000). Intravenous glucose tolerance tests performed on 30 orangutans ranging in age from 3.5-40.5 years revealed two diabetic and two potentially prediabetic individuals. Mean ± SE fasting plasma or serum glucose and insulin concentrations were 113 ± 16 mg·dl-1 and 45 ± 7 µU·ml-1, respectively. The two diabetic orangutans had fasting glucose concentrations of 380 and 562 mg·dl-1 and fasting insulin concentrations of 21 and 14 µU·ml-1. Their insulin responses during the intravenous glucose tolerance tests were low or non-detectable. Nearly half of all orangutans exhibited delayed or attenuated acute insulin responses.