Genetic regulation of plasma corticosterone concentration and its response to castration and allogeneic tumour growth in the mouse.

Abstract

EXCESS fat deposition after castration is thought to be a response to hyperinsulinism induced by an increased level of adrenal glucocorticoids1. Two mutant alleles, lethal yellow (Ay) and viable yellow (Avy), at the agouti locus in the mouse induce excess fat deposition; the Ay allele has also been found to induce insulin resistance2. Katsh3 concluded that in adrenalectomized KL strain mice a considerable portion of the high insulin tolerance depended on normal adrenal function. In the inbred YS/Wf and VY/Wf strains, both yellow pheno-types modulate serum insulin concentration4. Castration of inbred YS strain males causes a large decrease in serum insulin4, suggesting a possible relationship1 to the concentration of adrenal glucocorticoids. Growth of allogeneic tumour cells has different effects on the serum insulin concentrations of YS and VY strain mice4.