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Placental Lactogen and Growth Hormone Receptors in Human Fetal Tissues: Relationship to Fetal Plasma Human Placental Lactogen Concentrations and Fetal Growth^*

Department of Paediatrics, University of Sheffield, Clinical Sciences Centre, Northern General Hospital Sheffield S5 7A U, United Kingdom
The Department of Pediatrics, Duke University Medical Center (M.F., S.H.) Durham, North Carolina 27710

Address all correspondence and requests for reprints to: Dr. D. J. Hill, Department of Paediatrics, University of Sheffield, Clinical Sciences Centre, Northern General Hospital, Sheffield S5 7AU, United Kingdom.

The specific binding of human placental lactogen (hPL) and human GH (hGH) to particulate cell membranes from human fetal liver and skeletal muscle at 12–19 weeks gestation was examined. Fetal liver and muscle specifically bound [¹²⁵I]hPL. This binding was inhibited by increasing concentrations of unlabeled hPL (half-maximal concentrations, 2.2 and 3.4 nmol/L, respectively). Scatchard analysis of the hepatic membrane binding revealed curvilinear plots with higher (K_d, 2.2 nmol/L) and lower (K_d, 24 nmol/L) affinity sites, while binding to muscle involved a single receptor class of K_d 5.6 nmol/L. The binding capacities for the two hepatic sites correlated positively with fetal body weight. [¹²⁵I]hGH specifically bound to liver, but not muscle, with higher (K_d, 1.6 nmol/L) and lower (K_d, 8.6 nmol/L) affinity sites. [¹²⁵I]PRL bound to hepatic membranes, but was preferentially displaced by hPL or hGH. Between 4 and 500 µg/L (mean, 82 µg/L, 3.8 nmol/L) hPL were present in fetal plasma. The findings identify distinct hPL receptors in human fetal liver and skeletal muscle and a hepatic hGH receptor in midgestation.

^* This work was supported by the Yorkshire Cancer Research Campaign, Birthright, the Smith Kline Foundation, NIH Grants HD-00656 and HD-07447, and Basil O’Connor Starter Grant 5-503 from the March of Dimes.

Received September 22, 1987.

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