Experimental Hypersomatotropism - II. Metabolic Effects in Rats Bearing the MtT-W15 Tumor[*] [**]

Abstract

Hypersomatotropism was induced in Wistar/Furth female rats by inoculation of MtT-W15 tumor. Anatomical changes were reminiscent of those of acromegaly or juvenile gigantism. Nineteen days after tumor inoculation the circulating GH rose significantly above control level, and this rise was accompanied by increased concentration of FFA and blood acetone bodies. Hyperinsulinemia followed a few days later. Values of serum FFA and acetone bodies peaked in the early stage of hypersomatotropism. The early rise of serum FFA and later return towards normal levels suggested that FFA are rapidly oxidized or re-esterified in hypersomatotropism. GH caused a decreased glycogen synthesis in the diaphragm in vitro after insulin stimulation. This finding showed that GH caused peripheral insulin antagonism. The specific activity of the seromucoid fraction from rat plasma was decreased by 50% of the control values when glucosamine-1-¹⁴C was used. No decrease in the specific activity of seromucoid or perchloric acid insoluble fractions were observed when valine-U-¹⁴ was used. The implications of altered intermediary metabolism in the liver of tumor rats are discussed.

Key words

MtT-W15 Tumor - Hypersomatotropism - Hyperinsulinemia - Insulin Antagonism - Plasma Glycoproteins

1 Supported by Grant MT-1202 from the Medical Research Council of Canada.

2 Presented in part at the Third International Congress of Endocrinology, Mexico City, July 1968.

1 Supported by Grant MT-1202 from the Medical Research Council of Canada.

2 Presented in part at the Third International Congress of Endocrinology, Mexico City, July 1968.

3 Research Fellow, Medical Research Council of Canada. Present address: Children's Hospital, University of Helsinki, Helsinki 29, Finland.