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A colony of NZW rabbits was developed in which 18 of 126 members exhibited overt symptoms of diabetes mellitus. On the basis of total body weight measurements, obesity does not appear to play a primary role in the development or manifestation of the syndrome. The relatively high frequency of occurrence of spontaneous diabetes mellitus in this colony seems to suggest a unique genetic predisposition of these rabbits, yet analysis of glucose tolerance of colony animals indicates no clear genetic mode of transmittance of the trait. Rather, data suggest a possible interaction of as yet undefined genetic and/or environmental influences as being responsible for the disease state. Regressions of k-value on age indicate an early predetermination of glucose intolerance in the rabbits. In addition to a planned program of breeding, investigations of dietary intake and possible relationships of the diabetic condition to bacterial or viral infections appear to be initial areas indicative of further study.

Amygdalotomized, sham-operated and intact wild-derived house mice of both sexes were group-caged (8–10) or singly caged for 3 weeks. The weights of ovaries (p < 0.05) and uteri (p < 0.01) were less in intact and sham-operated grouped females compared to singly caged intact and amygdalotomized females. The weight of the reproductive organs in amygdalotomized grouped female mice was not different from singly caged controls. Body weights among amygdalotomized grouped females were heavier (p < 0.05) than singly caged controls. Seminal vesicle weights of intact and sham-operated grouped males were less (p < 0.05) than that of singly caged controls and grouped amygdalotomized males. Plasma LH values from the various groups coincided with the morphological data. These results support the hypothesis that increased population density impairs reproductive function in mammals. Perhaps the effects of decreased pituitary-gonadal function associated with overcrowding are mediated via amygdalar nuclei.

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