Ovarian–splenic autotransplantation: evidence that oestrogen does not inhibit hepatic somatomedin generation

Abstract

This study was designed to test the hypothesis that oestrogens inhibit growth by reducing hepatic somatomedin generation. We have attempted to deliver oestrogen preferentially to the liver by transplanting ovarian tissue into the spleen. Four groups of rats were compared: intact, ovariectomized, ovariectomized with successful ovarian transplants, and animals where due to adhesions between the transplant and body wall and/or viscera oestrogens reached the general circulation. Plasma levels of LH and FSH, uterine weights, ovarian weights and vaginal smears supported this classification of animals. Ovariectomy increased body weight, body length, bioassayable serum somatomedin levels and 35SO4(2-) uptake into costal cartilage in vivo compared with intact rats and animals with adhesions. Preferentially exposing the liver to oestrogen did not suppress the increased growth, serum somatomedin activity or uptake of 35SO4(2-) in vivo observed in ovariectomized animals. The results suggest that the presence of oestrogen in the general circulation is associated with growth suppression and lowered somatomedin bioactivity while the presence of oestrogen in the hepatic portal circulation has little effect on body growth. We conclude that oestrogen does not appear to inhibit growth in the rat by influencing the release of somatomedin from the liver. It also seems that serum somatomedin concentration may not reflect liver somatomedin generation but overall production throughout the body.

Actions of Immunosuppressor Drugs on the Development of an Experimental Ovarian Tumor1

“…In this new anatomic location, the steroids produced by the ovary reach the hepatic portal vein and are metabolized in the liver, In this way, the negative feedback normally exerted by the steroids on the hypothalamic-pituitary unit is abolished, and hypergonadotropinemia is established. The grafted ovary turns into a highly luteinized tumor (luteoma) under the constant stimulation of gonadotropins, which induce growth and hormonal activity (5,9,10). The dependency of this experimental luteoma on gonadotropin hyperstimulation for its growth is similar to the one observed in different ovarian pathologies as in certain ovarian carcinomas (11-13), granulosa-cell tumors after ovarian stimulation in treatments of infertility (14), or in the polycystic ovary syndrome (15,16) among others.…”

“…Tumors were measured in two dimensions with a caliper, and tumor volumes were calculated based on an ellipsoid tumor shape (V: 4/31T. r)2. r2' where r l is the minor radius (10,27). Some tumors of each group were placed in formaline for histological studies.…”