Delayed appearance of liver growth hormone binding sites and of growth hormone-induced somatomedin production during rat development.
The present study was designed to determine whether the apparent paradox of high circulating growth hormone levels in the fetus and the minimal effect of this hormone on growth might reflect a diminished responsiveness of fetal target organs to GH. Specific uptake by rat liver of [125I] bGH was very low in fetuses as compared to suckling and adult rats. Also, liver uptake of the iodinated hormone decreased proportionally with the simultaneous injection of increasing amounts of growth hormone, but was not modified by the simultaneous injection of unlabelled chemically-related hormones. Since the water content is significantly greater in fetal than adult tissues, results were expressed by liver dry weight and again, [125I] bGH liver uptake continued to increase with age. After bovine growth hormone administration to adult rats, plasma somatomedin C concentrations increased significantly, while they had no effect in fetuses. These results suggest that reduced liver somatogenic binding sites in the fetus prevents growth hormone from inducing growth-promoting effects during intrauterine life.
D000818:Animals; D000833:Animals, Suckling; D001665:Binding Sites; D002417:Cattle; D005260:Female; D013006:Growth Hormone / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology; D008099:Liver / Q000196:embryology / Q000378:metabolism*; D008297:Male; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains / Q000254:growth & development*; D013002:Somatomedins / Q000096:biosynthesis*; D013997:Time Factors
D007328:Insulin; D013002:Somatomedins; D013006:Growth Hormone