Abstract
Smith 1 produced obesity in rats by injecting chromic acid into the hypophysis via a subtemporal approach. Because hypophysectomy did not bring about the same result, Smith reasoned that hypophyseal deficiency could not be responsible for the adiposity—and that hypothalamic damage incurred during the chromic acid operation must have been the cause. Ranson, Fisher, and Ingram 2 have reported the effect of hypothalamic lesions on fat deposition in a large number of cats and monkeys observed in our laboratory, and lately the guinea pig has been added to this list. In all 3 species the results have been negative.
In an effort to discover the reason for this divergence of findings we have repeated, with modifications, Smith's chromic acid injections on rats. About 0.01 cc of 5% chromic acid was injected through a needle with a curved tip into the hypophyses of albino rats via a parapharyngeal approach. Using this method we hoped to minimize the danger of simultaneous hypothalamic damage. We have also placed lesions in the hypothalami of rats with the Horsley-Clarke instrument. Two electrolytic lesions were placed on each side in the lateral hypothalamic areas between the levels of the optic chiasma rostrally and the infundibulum caudally.
All rats were operated at about the time of sexual maturity. They had litter mate controls, and were allowed to survive well over the maximum time elapsing before any obese rat showed definite signs of its disorder. They were weighed at weekly intervals. At autopsy the brains were fixed in formalin, and the hypophyses in either Zenker-formol or Champy fluid. Serial sections of the hypothalami and neighboring areas were cut and stained with cresyl violet; the hypophyses were stained by either the Haterius modification of the Masson stain, or by the Severinghaus technic.
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