Dietary tyrosine supplementation corrects tyrosine and dopamine deficits in diabetic rat retina

Abstract

The dietary amino acid tyrosine is the precusor of the brain and retinal catecholamine transmitter dopamine (DA). Alterations in tissue level of this precursor may influence the rate at which the catechol is synthesized and released, particularly when the rate-limiting enzyme, tyrosine hydroxylase (TH), is activated. Physiologically, TH is activated in the retinal amacrine DA cell during exposure to light. In diabetic rats we have found that retinal tyrosine level is severely reduced and tyrosine supplementation of the diet can correct this deficiency and hence retinal DA. Retinal tyrosine level in streptozotocin-diabetic male rats was reduced to 0.24 ± 0.05 μg/mg protein from control levels of 0.71 ± 0.02 μg/mg protein. Addition of 4% tyrosine to the 24% casein basal diet increased tyrosine level threefold in both control (to 2.38 ± 0.30 μg/mg protein) and diabetic retina (to 0.62 ± 0.08 μg/mg protein). Retinal DA was also reduced in diabetic rats (controls, 2.23 ± 0.19 ng/mg protein; diabetic, 1.71 ±0.12 ng/mg protein) and this deficit was reversed by the addition of dietary tyrosine (2.12 ± 0.05 ng/mg protein).