Taurine in the central nervous system and the mammalian actions of taurine

Taurine: An overview of its role in preventive medicine

Diabetic neuropathy results from progressive nerve fibre damage with blunted nerve regeneration and repair and may be complicated by nerve hyperexcitability resulting in pain. The naturally occurring amino acid taurine functions as an osmolyte, inhibitory neurotransmitter, and modulator of pain perception. It is also known to have neurotrophic actions. The compatible osmolyte hypothesis proposes that levels of intracellular organic osmolytes including taurine and myo-inositol, respond co-ordinately in response to changes in intracellular sorbitol or external osmolality to maintain the intracellular milieu. We hypothesize that glucose-induced sorbitol accumulation in diabetes mellitus will result in taurine depletion in peripheral nerve which may potentially impair nerve regeneration and precipitate neuronal hyperexcitability and pain. This study explored the relationships of taurine, myo-inositol and sorbitol in the rat nerve and their effects on nerve conduction velocity. Osmolyte levels and nerve conduction velocity were determined in sciatic nerve from non-diabetic and streptozotocin-induced diabetic rats, with or without dietary taurine or myo-inositol supplementation. Taurine levels decreased by 31% (p< 0.01) and myo-inositol decreased by 37% (p<0.05) in diabetic nerve as sorbitol accumulated. Taurine supplementation of diabetic animals did not affect nerve conduction velocity but further reduced nerve myo-inositol levels. Prevention of sorbitol accumulation with the aldose reductase inhibitor sorbinil increased nerve taurine levels by 22% (p<0.05) when compared with untreated diabetic animals. Thus, we have demonstrated an interdependence of organic osmolytes within the nerve. Abnormal accumulation of one osmolyte results in reciprocal depletion of others. Diabetic neuropathy may be an example of maladaptive osmoregulation, nerve damage and instability being aggravated by taurine depletion.

/pdf/osmotically-induced-nerve-taurine-depletion-and-the-4qormji7u9.pdf

Osmotically-induced nerve taurine depletion and the compatible osmolyte hypothesis in experimental diabetic neuropathy in the rat.

More than simply cataloging the numerous experimental models in which taurine plays a modulating role, this discussion aims at stimulating further investigation of the potential clinical value of this abundant sulfur amino acid. Both the biomedical investigator and clinician must be struck by the enormous amount of taurine floating freely in the intracellular water of the cells. In cardiac tissue alone, taurine levels of 20 mM or higher may be found.2, 3 Given this abundance of taurine, why is our understanding of its function so elusive? Although it is clear taurine is important in conjugating bile acids to form water-soluble bile salts, only a fraction of available taurine is used for this function, predominantly in young animals and children. While taurine conjugation is the preferred route of bile acid conjugation in the young, changes in adults given 250 mg of taurine daily for two to three weeks are insignificant. Total pool size of bile acid and chenodeoxycholic acid declines. Unchanged are the rate of bile acid synthesis or the secretion rates of biliary cholesterol, bile acid and phospholipids. Biliary cholesterol saturation also stays the same.152 The finding that taurine availability protects against cholestasis induced by monohydroxy bile acids remains confined to guinea pigs.153 The abundance of taurine suggests it may be an osmoregulator of cell volume, and there is convincing evidence that it serves this function in fish. Taurine may play this role in the brain under high osmotic states such as hypernatremia, dehydration and uremia. Evidence is strong that taurine is vital in maintaining retinal function, which may explain why taurine is so abundant in human breast milk. Prolonged TPN feeding of infants demonstrates the importance of taurine in retinal development. We have begun to appreciate the role of the kidney in conserving taurine and how this is perturbed in the neonatal period. Taurine has recently been added to infant formulas (about 50 mg/L). Cataloging what we know of taurine function, however, produces a list of “maybes.” Now is the time for exhaustive, careful taurine research that will produce more definite answers. 

Taurine: Its Biological Role and Clinical Implications

Using a clonal growth assay, we demonstrated that taurine, a nonperturbing osmolyte accumulated in kidney medulla, brain, and some other tissues of hypertonic experimental animals can function as a nonperturbing osmolyte in Madin-Darby canine kidney (MDCK) cells. The taurine content of hypertonic MDCK cells is twice that of isotonic MDCK cells (isotonic 160 nmol/mg protein; hypertonic 320 nmol/mg protein). Therefore we studied taurine transport in MDCK cells grown on porous supports and then studied the effect of hypertonicity which is known to elicit increased uptake of some other nonperturbing osmolytes by MDCK cells. Basal uptake exceeded apical uptake, with Km and Vmax of 56 microM and 933 pmol/min.mg protein on the basal surface and 10 microM and 50 pmol/min.mg protein on the apical surface. On both surfaces, virtually all taurine uptake was Na+ and Cl- dependent. 24 h after cells were shifted to hypertonic medium (500 mosmol/kg), taurine uptake doubled on the basolateral surface without change on the apical surface. The response to hypertonicity was the result of an increase in Vmax without change in Km. There was no change in taurine efflux when cells were shifted from isotonic to hypertonic medium. When cells adapted to hypertonic medium were shifted to isotonic medium, a large transient basolateral efflux of taurine occurred within 10 min. We conclude that taurine can function as a nonperturbing osmolyte in MDCK cells and that tonicity-regulated taurine transport is a basolateral function in MDCK cells.

/pdf/taurine-behaves-as-an-osmolyte-in-madin-darby-canine-kidney-u0ks7t2j2j.pdf

Taurine behaves as an osmolyte in Madin-Darby canine kidney cells. Protection by polarized, regulated transport of taurine.

The relative contribution of diet and biosynthesis to the taurine content of the rat has been determined quantitatively under various dietary conditions. Rats were maintained on diets containing [3H]taurine and/or [35S]methionine of known amounts and specific activities, and subsequently the specific activity of taurine in various tissues was determined. This approach gives a quantitative measure of how much taurine is biosynthesized versus how much is derived from the diet regardless of the biosynthetic route or site of biosynthesis in the animal. With no taurine in the diet, over an 87-day period, 54% of the taurine in the animal had been biosynthesized. This fell to 29% if taurine was present in the diet, and the contribution of dietary taurine to body pools rose to 58%. These changes in biosynthetic contributions were not accompanied by an alteration in the rate of biosynthesis but by an alteration in rate of excretion. When the amounts of biosynthesized taurine appearing in the urine over 63 days was added to the amounts found in the carcass, 3.1 mmol were found to be biosynthesized by animals receiving taurine in the diet as compared to 2.9 mmol in animals on a taurine-deficient diet. In any one experiment, the contribution of diet or biosynthesis is invariant from tissue to tissue indicating that the rate of exchange of taurine between tissues is faster than the rate of elimination of taurine from the body.

Relative contribution of diet and biosynthesis to the taurine content of the adult rat.

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Relative contribution of diet and biosynthesis to the taurine content of the adult rat.