Placental lactogen administration reverses the effect of low-protein diet on maternal and fetal serum somatomedin levels in the pregnant rat.

Female rats were studied on day 20 of pregnancy after being fed either a 5% lactalbumin (low protein) diet or a 20% lactalbumin (adequate) diet for the last 2 weeks of pregnancy. Rats on the lower intake of protein showed decreased serum levels of rat placental lactogen and reduced numbers of lactogenic receptors in the maternal liver. These changes were accompanied by much reduced serum levels of somatomedins IGF I(insulin-like growth factor) and II (multiplication-stimulating activity, MSA). Infusion of human placental lactogen or human growth hormone into the rats on the low-protein intake during the last 2 weeks of pregnancy partially restored the maternal serum levels of both somatomedins, but only human placental lactogen increased the number of lactogenic receptors on liver cell membranes. It was concluded that protein deficiency may reduce secretion of somatomedins by the liver (or other tissues) of the pregnant rat indirectly through reduction in output of rat placental lactogen by the placenta. In the same experiments, the effect of maternal protein deficiency on fetal development and serum somatomedin levels was examined. Protein deficiency resulted in smaller fetuses and placentas and lower fetal serum levels of IGF I and MSA. Unlike the response in maternal serum levels, the concentration of MSA in the fetal serum increased during infusion of hPL or hGH but the concentration of IGF I did not. This suggests that placental lactogen enters the fetal circulation and affects tissues producing MSA but not those making IGF I. Despite the restoration of MSA levels, fetal and placental weights did not increase when the rats on the protein-deficient diets were treated with human placental lactogen or growth hormone.