Onset of obesity and puberty in genetically obese SHHF/Mcc-cp rats.

SHHF/Mcc-cp rats, as a model of obesity and diabetes, were followed through breeding and throughout development to determine timing of obesity and sexual development. The obesity or corpulency gene (cp) follows recessive transmission characteristics with no segregation between sexes. Although the frequency of litter sizes was different, the mean litter size of heterozygous mating (8.9 +/- 0.3 pups/litter) was not different from homozygous lean matings (7.9 +/- 0.3 pups/litter). Body weights of the population of female obese rats statistically deviated from lean females at day 35 and obese males deviated from lean males at day 37. Vaginal opening of obese and lean females did not differ in time of occurrence (day 34.6 +/- 0.2 for lean and 33.6 +/- 0.4 for obese). To further evaluate development and examine onset of diabetes, animals were killed at six, eight and ten weeks of age and development of reproductive organs and plasma levels of insulin, glucose, and testosterone or oestradiol determined. Testes development was slightly retarded in the obese male with smaller testes at six weeks of age, however testes size increased at eight and ten weeks of age and was not significantly less than lean males. In contrast, testes function was impaired with smaller seminal vesicles and lower testosterone levels in the obese male rats. Both ovarian and uterine weights were significantly less in obese females. However, oestradiol levels were not significantly different at any of the time points examined. Development of elevated insulin levels were first noted in the obese female at six weeks of age, however marked hyperinsulinemia developed only in the obese males at ten weeks of age.(ABSTRACT TRUNCATED AT 250 WORDS)