Hyperlipemia in Infant Monkeys Fed Excess L-Histidine. ∗

Abstract

The ability to induce hyperlipemia in small laboratory animals by a variety of experimental conditions has advanced the knowledge of lipid metabolism in health and disease. The advantage of utilizing the subhuman primate in such studies is self-evident if the data are to be meaningful in terms of the human. Monkeys have provided valuable information relating lipid metabolism to atherosclerosis(1) and the development and progression of the atheromatous lesion in the monkey closely parallels that observed in man(2). Many investigations have shown that the blood lipid level in the subhuman primate quickly reflects alterations in total cholesterol content of the diet(3). It seemed of importance, therefore, to report that hyperlipemia in the infant monkey could also be produced by feeding excess quantities of L-histidine without modifying the dietary lipid. This was especially interesting because hyperlipemia had not been noted in this laboratory when large numbers of rhesus monkeys were fed other amino acids in excess quantities (4,5). Materials and methods. Experiments with L-histidine were performed on 4 infant rhesus monkeys (M. mulatta) of known genetic background and gestational age, which were removed from their mothers on the date of birth and placed in individually heated cages. The infants weighed between 410–570 g at birth and were considered normal in all respects. These infants were maintained in a metabolic nursery under 24-hour observation and care. They were fed at 4-hour intervals, at first by hand, then ad libitum, a commercial milk mixture† which was similar in composition to human and monkey breast milk. Daily dietary intake and growth records were kept and blood and urine collections(4) were obtained at appropriate intervals. The infant monkeys did not receive any lipid, carbohydrate, or protein other than that provided by the milk preparation and by supplements of vitamins and fruits.