The Biochemical Defect Underlying the Nutritional Failure of Young Rats on Diets Containing Excessive Quantities of Lactose or Galactose

Abstract

Weanling rats of the Vanderbilt strain die within 3 to 17 days after being placed on diets containing more than 60% lactose or 40% galactose. No lesions other than those associated with simple inanition were found by histological examination of their tissues. While most rats exhibited a marked diarrhea and all a profound diuresis, death did not appear to have been due to dehydration or acidosis. While all rats had a marked calcinuria due to the enhanced calcium absorption from the intestine, their serum calcium concentrations were only moderately elevated and did not appear to be an etiologic factor in the death of such rats. Moribund rats on both lactose and galactose diets were found to have blood galactose concentrations varying from 210 to 640 mg % with true blood glucose levels which varied from 26 to 73 mg %. Simultaneously there occurred an appreciable drop in the serum inorganic phosphorus concentration and almost complete depletion of the liver glycogen. It is concluded that this disturbance of carbohydrate metabolism, which is similar to that occasionally observed in infants while they drink milk, is the prime etiologic factor in the death of rats on such diets. The occasional “galactosemia” seen in infants is thought to represent not a qualitative idiopathic phenomenon but a quantitative exaggeration of events which can be elicited in a normal animal when the galactose intake is sufficiently high. The mechanism whereby galactose interferes with normal glucose metabolism has not yet been clearly defined.