Ontogeny of Liver Somatotropic and Lactogenic Binding Sites in Male and Female Rats*

Developmental changes in liver somatotropic (GH) and lactogenic (PRL) binding sites were evaluated in male and female rats from birth to sexual maturity, and compared with growth velocity, plasma GH, PRL, testosterone, and estrogens. The affinity (Ka) and the concentration of these sites were determined from the analysis of equilibrium saturation curves with [125I]bovine GH and [125I]ovine PRL, incubated with liver homogenates. GH receptors rose from 6.4 fmol/mg protein at 8 days of age to 30.3 fmol/mg protein in males and 39.4 fmol/mg protein in females at 28 days. This surge occurred concomitant with the fall of plasma GH observed after birth. It preceded by about 1 week the acceleration of growth velocity and the increase of plasma GH seen at puberty. After the peak of growth velocity (42 days), GH receptors increased steadily until 120 days in females (63.8 fmol/mg protein), whereas in males they reached a concentration of 33.5 fmol/mg protein after a transient decrease to a nadir of 13.3 fmol/mg protein a day 50. From day 8 to day 35, PRL receptors in males remained at a constant level of 10.3 fmol/mg protein, whereas in females they increased progressively from 4.8 to 21.5 fmol/mg protein. Thereafter, in most pubertal males, they became undetectable, whereas plasma testosterone was rising. In contrast, PRL receptors in females increased 3-fold between day 42 (18.9 fmol/protein) and day 50 (50.2 fmol/mg protein). Between days 8 and 120, the Ko of GH and PRL receptors showed no significant changes with age and sex (GH: 0.66 x 109 M−1; PRL: 0.97 × 109m−1). In conclusion, the rise of liver GH receptors occurring before puberty in male and female rats may be of importance for the initiation of the pubertal growth spurt. The inverse relationship between plasma testosterone and liver PRL receptors in pubertal male rats suggests that physiological concentrations of testosterone may inhibit PRL receptors. In contrast, in female rats an opposite change of PRL receptors is observed during puberty. (Endocrinology113: 1325, 1983)