GROWTH-HORMONE (GH) MODULATES INSULIN-LIKE GROWTH-FACTOR-I (IGF-I) AND TYPE-I IGF RECEPTOR MESSENGER-RNA LEVELS IN THE OVARY OF PREPUBERTALGH-DEFICIENT RATS

In order to explore the potential role of growth hormone (GH) in modul ating insulin-like growth factor I (IGF-I) gene expression in the prep ubertal rat ovary, female rats were rendered GH deficient by neonatal administration of monosodium glutamate (MSG). One group of rats receiv ed vehicle and served as the control. At 21 days of age, MSG-treated r ats received either GH or vehicle for 2 weeks. On days 21, 24, 28 and 31 animals were weighed and subsets were sacrificed for liver RNA extr action. The remaining animals were sacrificed at day 35 when livers an d ovaries were collected, and serum was obtained for GH determinations . The IGF-I mRNA levels were estimated by Northern blots and corrobora ted further by slot-blot analysis. The MSG-treated rats had lower body weights (p < 0.01) and GH levels (p < 0.05) than controls. Growth hor mone replacement significantly accelerated the weight gain of MSG-trea ted rats. At day 24 and thereafter, three RNA IGF-I species (7.5, 1.8 and 0.8-1.2 kB) were seen in the liver. in the ovary, at age 35 days, two major IGF-I mRNA species (7.5 and 0.8-1.2 kb) were seen. The MSG t reatment consistently reduced the levels of both IGF-I mRNA species in the ovary. Growth hormone administration partially restored their exp ression, both in the liver and in the ovary. In addition, ovarian type I IGF receptor mRNA levels were increased in the MSG-treated rats whe n compared to controls. This trend was reversed by GH replacement. In summary, we have found that in prepubertal female rats rendered GH def icient with MSG, ovarian IGF-I gene expression is reduced while type I IGF receptor mRNA levels are increased. These findings are reversed w ith GH replacement. These results suggest a physiological role for GH in modulating IGF-I and type I IGF receptor genes in the ovary.