Human infants fed commercial formulas which contain little or no taurine have reduced plasma taurine concentrations compared to similar infants fed human milk, which is rich in taurine. Cats fed taurine-free synthetic diets become taurine-depleted and suffer retinal degeneration, tapetal degeneration, and severely impaired visual function. These gross effects are easily detectable ophthalmoscopically and electrophysiologically, and the changes at the ultrastructural level are profound. Cats that are partially taurine depleted suffer changes in membrane morphology that can be detected only with high magnification electron microscopy. A preliminary study with infant rhesus monkeys raised on a human infant protein hydrolysate formula indicated that this species may be a good animal model for human infants. We found decreased plasma taurine concentrations, similar to those observed in human infants, and no ophthalmoscopically visible abnormalities. At 10 months, cone-dominated ERG's were significantly reduced, but rod-dominated responses were unchanged. By 18 months, these changes were no longer significant. At 26 months, ultrastructural examination showed consistent disorientation and vesiculation of disc membranes in the outer segments of cones, but not in rods. Such changes were not observed in animals receiving the same formula supplemented with taurine. We propose to examine the effect of feeding a human infant soy protein formula, with and without taurine supplementation, to infant rhesus monkeys. Blood will be sampled periodically for amino acid analysis, electroretinograms and visual evoked potentials will be recorded at 3-monthly intervals, visual acuity will be measured behaviorally, and animals will be sacrificed at 3, 6 and 12 months for examination of amino acid content of tissues and for ultrastructure of retina and brain. A further group will be supplemented with taurine after 3 or 6 months on formula alone and killed 6 months later to examine the degree of reversibility of the changes. Other recent results have implicated nutritional taurine in the normal postnatal migration of cerebellar granule cells. The results of this study should allow a recommendation to be made regarding the addition of taurine to human infant formulas. This question assumes special importance now that retinal damage associated with taurine deficiency has been documented in human infants and children.
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