Prolactin modifies the fluidity of rat liver membranes.

Summary The objective of this study was to determine the effect of prolactin upon the fluidity of hepatic membranes and subsequent modification of the prolactin receptors. Hypophysectomized, immature, female rats (HIFR) having subcutaneous diethyl stillbesterol implants were treated with pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG). In addition, graded doses of 0, 0.25, 0.5, 1.0, 2.5 or 50 μg oPRL were injected hourly for the 48 hours prior to sacrifice at 28 days of age. Both the lipid fluidity as determined by 1,6-diphenylhexatriene (DPH) fluorescence polarization and phospholipid/cholesterol (P/C) ratio were measured in hepatic microsomal membranes. A biphasic response was observed in both of these parameters as the dose of oPRL was increased. P/C values were 91,113, 117, 88, and 93% of control values for the 0.25, 0.5, 1.0, 2.5 and 50 μg oPRL groups, respectively, the maximal value being significantly different from the saline injected controls. These ratios were inversely proportional to the corresponding values of fluidity which also varied in a biphasic manner, with fluorescence polarization equal to 97, 90, 82, 100 and 101% of control values. The value for the 1.0 μg group was, again, significantly different from control. No significant specific 125 I-oPRL binding was detectable in any of the groups after treating the membranes with distilled water, however, pretreatment of membrane preparations with 4 M MgCl 2 for 5 min resulted in a significant increase in the oPRL-binding in the 0.5 and 1.0 μg oPRL groups. The values being 273 and 521% of control, respectively in these two groups. These data demonstrate that prolactin modifies the viscosity of hepatic membranes and suggests that this phenomenon may be responsible for the autoregulation of detectable prolactin receptors.