Response of a Pituitary Tumor to Thyroid Hormone

Publisher Website
Google Scholar
Abstract
Administration of pro-pylthiouracil to rats bearing pituitary tumor MtTW5, decreased the rate of tumor growth. When thyroidectomized rats were inoculated with pituitary tumor, no growth of the tumor was observed, nor were any of the hormonally produced effects found. Implantation of thyroid glands or administration of thyroxine caused a prompt restoration of pituitary tumor growth mammary, tumor growth, and a generalized increase in body weight. Thyroidectomy of rats bearing large pituitary tumor caused an immediate cessation of further tumor growth. Slices of liver from tumor-bearing rats were incubated in vitro with acetate -1-14C and produced ratioactive carbon dioxide and fatty acids at a faster rate than liver slices from normal rats. Whereas liver slices from thyroidectomized rats bearing MtTW5 inoculum, metabolized acetate-1- 14C at control rates, thyroxine stimulated pituitary tumor growth, which caused an increase in liver acetate metabolism. Retroperitoneal adipose tissue in pituitary tumor-bearing rats oxidized glucose-6-14C to 14CO2 and produced fatty acids at greatly diminished rates, whereas adipose tissue from thyroidectomized rats bearing pituitary tumor inoculum, metabolized glucose-6-14C at the same rate as did control tissue. Transplantation of thyroid glands into the thyroidectomized rats decreased carbon dioxide production and fatty acid biosynthesis. It is concluded that thyroid hormone is essential for the growth of a transplant-able pituitary tumor MtTW5 and for the changes in hormonal glucose and acetate metabolism.