EXPERIMENTAL OBESITY IN THE DOG

Abstract
Exptl. evidence shows that in the dog obesity results from bilateral destruction or retrograde degeneration of the paired paraventricular nuclei, particularly of their caudal portions. Marked obesity results when such condition coexists with destruction or denervation of the neuro-hypophysis. Removal of the pars distalis itself results in a slow wt. increase in the adult dog which becomes marked with time. The presence of the pars distalis in animals with the supraoptic and paraventricular nuclei destroyed or degenerated is favorable to the rapid development of marked obesity. Destruction or denervation of the caudal portion of the paraventricular nuclei leads to changes in the body which increase the food intake. The cells of the hypophysis become sensitive to the adrenal cortical hormone and probably this causes a marked loss of basophil cells in the glandular division of the hypophysis. This promotes changes in the thyroid and the gonads and probably indirectly influences the islet cells of the pancreas. The adrenals do not atrophy. The alterations in metabolism effected by such changes cause the accumulation of fat in various tissues of the body. Total and simple hypophysec-tomized dogs show, in addition to changes in the thyroid, the gonads, and the pancreas, an atrophy of the adrenal cortex. This may explain the fact that while they become obese, the rate of accumulation of fat and its amt. are less than in the "puncture dogs." Obesity is considered to result because of an excess of food intake over food requirement. The intake may be excessive because the metabolic needs are reduced by depression of thyroid or of gonad activity or of both together, while hunger is maintained; because an exaggerated hunger is induced by a downward shift in blood glucose caused by the exaggerated consumption of carbohydrate in the tissues, as in hypofunction of the hypophysis, or by exaggerated influences from the adrenal cortical hormone following an appropriate hypothalamic lesion. Changes in metabolism leading to obesity are quantitative rather than qualitative.