CHORIONIC GROWTH HORMONE‐PROLACTIN (CGP): SECRETION, DISPOSITION, BIOLOGIC ACTIVITY IN MAN, AND POSTULATED FUNCTION AS THE “GROWTH HORMONE” OF THE SECOND HALF OF PREGNANCY^*

Relations between Placental Concentrations of Chorionic Somatomammotropin (Placental Lactogen) and Growth: A Study Using the Twin Method

“…Nevertheless, there are individual differences within most of the twin pairs and this study has shown that these differences in placental HCS concentration and in total placental content of HCS are significantly related, not only to fetal growth, but to postnatal growth as well. The growth-promoting function of HCS as postulated by Grumbach et al [3] cannot explain the growth differences found in this study, as both twins in a pair share equally the benefits of maternal metabolic alterations induced by HCS. It is likely that these differences in placental HCS reflect differences in functioning syncytiotrophoblastic mass and thus represent an index of overall placental function sustaining fetal growth.…”

“…In the ensuing decade it has been established that HCS is secreted predominantly into the maternal circulation, producing alterations in maternal metabolism which are conducive to fetal growth [3].…”

Fetal rat lung epithelium has a functional growth hormone receptor coupled to tyrosine kinase activity and insulin-like growth factor binding protein-2 production

“…Prolactin receptors and placental lactogen receptors were once regarded as potential receptors for GH in the fetal compartment (Grumbach et al 1968). However, bGH does not bind to the rat prolactin receptor (Barash et al 1988) and binding studies using placental lactogen indicate that there are no binding sites for the placental lactogen receptor in fetal rat lung (Freemark et al 1993).…”

Human Chorionic Somatomamotraophin and Its Clinical Significance

“…Thus Teoh et al (1971) found a maximum difference of 15% from the mean of serum HCS values measured three times during the day, which could be accounted for by the error of the assay. Some workers find no change of serum HCS levels with hypo-or hyperglycaemia (Samaan et al, 1966;Grumbach et al, 1968) in marked contrast to serum HGH; others, however, find a slight but significant rise of serum HCS with hypoglycaemia, and conversely a fall with hyperglycaemia (Burt et al, 1970;Spellacy et al, 1971a). There is no change of serum HCS levels following the infusion of amino-acids (Tyson et al, 1969) or the ingestion of protein (Tyson et al, 1971b).…”

“…Its half life of disappearance has been estimated by several workers (Beck et al, 1965;Spellacy et al, 1966;Beck & Daughaday, 1967;Samaan et al, 1966;Singer et al, 1970) either following delivery or the injection of labelled HCS, as between 14.5 and 30 min. Grumbach et al (1968) report a double exponential disappearance pattern, the half life of the first component being 11.9-15.3 min and that of the second 47.1 min. Estimates of the daily secretion rate of HCS near term vary between 290 and 1800 mg (Beck & Daughaday, 1967;Kaplan et al, 1968), in contrast with the normal secretion rate of HGH of approximately 1 mg daily (Kowarski et al, 1971).…”