| Abstract: | In ob/ob mice a 12-wk period of food restriction led to a reduced rate of somatic growth and a decreased lean body mass, along with small but reliable reductions in systemic immunoreactive insulin levels and evidence of increased insulin sensitivity. However, no effects of limited access to food were noted on the basal hyperglycemia, the elevated percent carcass lipid, or on the significantly higher levels of serum corticoids that occur in obese animals. These data indicate that hyperphagia alone is not responsible for the maintenance of many of the commonly reported characteristics of the obese-hyperglycemic syndrome, but do not exclude the contribution of factors secondary to the quantity of ingested food. Additionally, the present data lend support to recent work suggesting that chronic hyperinsulinemia or an elevated set point of total carcass lipid may be instrumental in the development of this syndrome. |
