Tryptophan Deficiency in the Rat Induced by Forced Feeding of an Acid Hydrolyzed Casein Diet

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Abstract
Young and mature rats of both sexes of the Sprague-Dawley strain were force-fed three times daily an acidhydrolyzed casein diet deficient in tryptophan. The deficient diet was supplemented with 0.20% l-tryptophan for the control animals. Rats from both groups were sacrificed for chemical and histological examination at regular intervals to determine the progressive changes produced by tryptophan deficiency. The tryptophan-deficient rats exhibited a general alopecia, bloating and diarrhea. A peculiar behavior pattern was commonly observed after forced feeding, sometimes accompanied by convulsive fits which frequently ended in death. There were no significant changes in the dry matter, fat and nitrogen concentrations of the carcass. There was enlargement of the kidney, while the spleen atrophied. There was marked hypertrophy of the liver with a reduction in the nitrogen concentration, although the fat-free dry matter content was not significantly changed. A slight anemia was produced, which was also cured by tryptophan. There was degeneration of the semeniferous tubules in the testes of male rats. The previous finding of fatty infiltration of the liver was confirmed by both chemical analysis and histological examination, and, because the mitochondria in the cells of fatty livers were less numerous and different in size and shape from those of the control animals, it is probable that the fatty accumulation is a result of decreased fatty acid oxidase activity. This system of enzymes of the liver is located exclusively in the mitochondria. The changes in percentage weight of the liver and spleen were reversible, as was the fatty infiltration of the liver when curative treatment was initiated after 10 days on the deficient diet. Atrophy and degeneration of visceral and cardiac muscle are striking effects of tryptophan deficiency. Injury to epithelial tissues occurred in a few organs, but its importance appears limited. Keratinization of the cornea was recognizable after about 9 days of tryptophan deficiency and was usually accompanied by other ocular lesions, which have been adequately described by Albanese and Buschke ('42).