Lactogenic hormones stimulate the liver to secrete a factor that acts synergistically with prolactin to promote growth of the pigeon crop-sac mucosal epithelium in vivo.

We have investigated whether the liver is a source of a PRL-synergizing activity (i.e. synlactin) and we have obtained some information on endocrine control of its secretion. Livers were removed from 3-month-old Long-Evans rats (male, virgin, pregnant, or lactating female) or from virgin females that were injected with saline, bovine GH, or ovine PRL for 7 days, and hepatic slices were prepared for in vitro incubation in medium 199. The media were tested for synlactin activity by determining whether they could augment the pigeon crop-sac response to locally injected ovine PRL. Only the media containing factors from the liver of pregnant or lactating females and PRL-injected virgins had significant synlactin activity. They augmented the crop-sac mucosal growth response by 130%, 140%, and 103%, respectively. Medium in which slices of kidney from virgin or pregnant rats were incubated did not have detectable synlactin activity. The medium samples that had synlactin activity were also tested for the presence of bioactive (crop-sac assay) and immunoreactive (RIA) rat PRL, and none had detectable amounts of the hormone. Hence, the augmenting effect is not due to PRL that is sequestered in and released by the liver. The levels of insulin-like growth factor I/somatomedin-C in medium samples that did or did not have synlactin activity (from pregnant and virgin females, respectively) were measured by RIA and were found to be equivalent. Hence, synlactin activity is probably not due to insulin-like growth factor I. Overall, our results indicate that lactogenic hormones (i.e. pituitary PRL, and presumably placental lactogens in the pregnant rats) stimulate the liver to secrete synlactin activity. The hepatic PRL receptors which increase in number in pregnant females may be involved in the secretion of synlactin, which could then act in concert with ovarian steroids and GH and/or PRL to promote mammary growth.