Suppression of Receptors for Prolactin and Estrogen in Rat Liver Due to Treatment with the Growth Hormone Analogue Produced by the Tapeworm Spirometra Mansonoides

The rate of weight gain in the PGF-treated rats was accelerated in spite of a marked reduction in serum GH, and specific binding of [3H]estradiol in anterior pituitary was also suppressed by PGF treatment.

Abstract

Somatogenic hormones play an important role in regulation of receptors for prolactin (PRL) and estrogen. Plerocercoids of the tapeworm, S. mansonoides produce a factor which mimics some, but not all of the actions reported for GH. Intact female rats were subjected to a constant infusion of plerocercoid growth factor (PGF) via a subcutaneous infection for two weeks to determine if PGF influences receptors for PRL, GH or estradiol. The rate of weight gain in the PGF-treated rats was accelerated in spite of a marked reduction in serum GH. Partially-purified PGF specifically displaced [125I]hGH from rat liver receptors but microsomes prepared from rats treated with PGF specifically bound significantly less [125I]hGH than microsomes from control rats. The reduction in [125I]hGH binding was not due to occupancy or to a change in affinity but to a suppression in receptor concentration. Scatchard analysis of [3H]estradiol binding in rat liver cytosols shows a 50% reduction in receptor concentration in the PGF-treated group. Specific binding of [3H]estradiol in anterior pituitary was also suppressed by PGF treatment.