Growth hormone causes rapid induction of lactogenic receptor activity in the Snell dwarf mouse liver.

The Snell dwarf mouse (dw/dw) has no detectable PRL-binding sites in the microsomal fractions of its liver. Both bGH and bPRL, purified by preparative gel electrophoresis, induce PRL-binding sites when injected into dw/dw. Intraperitoneal injection of 100 micrograms bGH every 8 h results in the appearance of a high affinity PRL receptor 8--16 h after initiation of treatment. This induced binding capacity plateaus after 32 h of treatment and subsequently decreases to nondetectable levels 48 h after the last injection. [125I]Iodo-ovine PRL is displaced from the induced receptor equally well by similar concentrations of ovine PRL, human GH, and bovine PRL, but is displaced by bovine GH (bGH) only at approximately 100-fold higher concentrations. While untreated dw/dw livers do possess high affinity bGH-binding sites, treatment with bGH did not alter the bGH-binding activity. Treatment of dw/dw with cycloheximide does not prevent induction of PRL receptors by bGH injections. These observations indicate that bGH induces the PRL receptor by interacting with the cell at some point distal to the induced receptor site and does not require the synthesis of new proteins.