The results of this study indicate that aging is associated with progressive declines in the normal dietary and metabolic responses to diet and environment in this animal model. The normal thermic and hormonal responses to diet and environment are thought to contribute to the fine regulation of energy balance by modulation of the efficiency of energy utilization or storage [25]. In the obese phenotype, the declines in the above variables may be further complicated by the presence of long-standing insulin resistance, and by perturbations in the normal metabolism and action of thyroid hormones, particularly T3. These may further contribute, individually or in combination with other factors, to an enhancement of energy storage and thereby contribute to maintaining the obese state. Moreover, the effects of progressive increases in obesity further exacerbate the decline in the economy of energy utilization and storage. Thus the impact of these physiologic changes of aging and obesity may impart significant alterations on the efficiency of energy metabolism, which in turn may contribute to some of the pathophysiologic changes associated with longevity, and could influence nutritional indices in affected individuals. As nations become progressively more industrialized, the incidence of overweight conditions--including obesity, NIDDM, and related metabolic disorders--has been shown to become increased and, along with those changes, the metabolic and pathophysiologic sequelae related to those disorders become more common [6-8]. A greater understanding of mechanisms of impaired energy metabolism and energy balance in aging may provide new insight into the nutritional factors that may contribute to obesity in aging, their modulation, and the emergence of a longer, healthier lifestyle.

1. Adipose mass and cellularity were studied in congenic female SHR/N-cp rats fed iosenergetic diets containing 54% carbohydrate as sucrose (SU) or cooked cornstarch (CS), 20% protein, 16% mixed dietary fat plus vitamins, minerals, and non-nutritive fiber ad libitum from 5 weeks until 8.5 months of age. Measures of adipocyte lipid content, cell number per depot, and mass of principal white (WAT) and interscapular brown (IBAT) adipoe tissue depots were determined at the end of the study. 2. Final body weights (BW) of corpulent rats were more than twice those of their lean littermates, and were greater when fed the SU than the CS diet in both phenotypes. Phenotype effects (corpulent > lean) were present for fat pad weight, adipocyte number, and adipocyte lipid content in the dorsal (DOR) and retroperitoneal (RP) WAT depots. Diet effects were present for depot weight, adipocyte number, and adipocyte lipid content in both WAT depots, and were of qualitatively similar magnitude in both phenotypes. 3. IBAT weights, IBAT: BW ratios, and IBAT cell number of corpulent > lean, and were > with SU than CS diet in both phenotypes. 4. These results indicate that obesity in the corpulent phenotype of the SHR/N-cp rat occurs as the result of hypertrophy and hyperplasia of white adipose tissue, and that isoenergetic substitution of simple for complex carbohydrate resulted in greater fat accretion in both phenotypes. The greater diet and phenotype-associated adiposity occurred despite greater mass and cellularity of BAT. The results also indicate that sexual dimorphism occurs regarding effects of diet and phenotype on expression of adipose tissue development in this strain.