Care of premature infants often requires parental and caregiver separation, 
particularly during hypoxic and hypothermic episodes. We have established a 
neonatal rat model of human prematurity involving maternal-neonatal separation 
and hypoxia with spontaneous hypothermia prevented by external heat. Adults 
previously exposed to these neonatal stressors show a sex difference in the 
insulin and glucose response to arginine stimulation suggesting a state of 
insulin resistance. The current study used this cohort of adult rats to evaluate 
insulin resistance [homeostatic model assessment of insulin resistance 
(HOMA-IR)], plasma adipokines (reflecting insulin resistance states), and 
testosterone. The major findings were that daily maternal-neonatal separation 
led to an increase in body weight and HOMA-IR in adult male and female rats and 
increased plasma leptin in adult male rats only; neither prior neonatal hypoxia 
(without or with body temperature control) nor neonatal hypothermia altered 
subsequent adult HOMA-IR or plasma adiponectin. Adult male-female differences in 
plasma leptin were lost with prior exposure to neonatal hypoxia or hypothermia; 
male-female differences in resistin were lost in the adults that were exposed to 
hypoxia and spontaneous hypothermia as neonates. Exposure of neonates to daily 
hypoxia without spontaneous hypothermia led to a decrease in plasma testosterone 
in adult male rats. We conclude that neonatal stressors result in subsequent 
adult sex-dependent increases in insulin resistance and adipokines and that our 
rat model of prematurity with hypoxia without hypothermia alters adult 
testosterone dynamics.