Hansen S.H., 2001
Taurine has different physiological functions, for example in the formation of bile acid, such as osmolite for the regulation of cell volume, in the heart, in the retina, in the formation of N-chlortaurine by reaction of hypochlorous acid in leukocytes. In some animals such as cat and mouse strain C57BL/6, used widely as an animal model of human diseases such as diabetes and atherosclerosis, were found disorders in the homeostasis of taurine.
The formation and consequently the accumulation of intracellular sorbitol, typical in the presence of diabetes, most likely causes the depletion of intracellular compounds including osmolites such as Myo-inositol and taurine.
The altered metabolism of taurine and the development of cellular dysfunctions that cause clinical complications in diabetes, such as retinopathy, neuropathy, nephropathy, cardiomyopathy, platelet aggregation, endothelial dysfunction, and atherosclerosis, have often been associated, so much to assume therapeutic perspectives with the integration of taurine and other osmolites.
Taurine is found in high intracellular concentrations in most animal tissues and some algae, but its physiological role has not yet been understood, although in some carnivores it is involved in the transformation of cholesterol into water-soluble bile salts and it also appears to have a determining role in osmoregulation, in the central nervous system (CNS), in retinal function, in cardiac function and inhibition of protein phosphorylation.
The primary metabolic pathway for the synthesis of taurine in mammals occurs in the liver in the cysteine sulfinic acid pathway. In this way, the sulfide group of cysteine is initially oxidized to cysteine-sulfinic acid by the enzyme cysteine diossigenase. The cysteine sulfinic acid is decarboxylated by cysteine-acidosolfinic decarboxylase for the formation of hypotaurine.
Beyond this primary biosynthetic pathway, more in-depth studies have observed the formation of taurine through biosynthetic pathways in other tissues, highlighting a synthesis capacity and a rate of reciclage of the same, which is variable in the various mammals. For example, in the rat and in the mouse there are very high biosynthetic capacities of taurine, whilst it is limited in the man and almost absent in the cat.
In biochemistry the only reference to taurine is the well-known biological function in the metabolism of cholesterol when the cholic acid is conjugated with taurine or glycine to form bile acids respectively, such as: taurocolic acid and glycocolic acid. The ratio of bile acids conjugated with glycine and taurine varies between mammals, for example almost exclusive conjugation of taurine in the rat. Glycine and taurine conjugates with a ratio of 3:1 are observed in humans and it has been shown that oral administration of taurine greatly increases the relative amount of taurocolic acid in bile. The bile salts participate in the absorption of fat in the intestine and are only partially reabsorbed. This excretion of bile salts is the only route of excretion of cholesterol from the body, which most likely occurs mainly with taurocolic acid. It follows from this that taurine deficiency will reduce the excretion of cholesterol, causing its accumulation in the body and consequently increasing the risk of atherosclerosis.
Immunocytochemical studies have shown very high concentrations of taurine and cysteine sulfin decarboxylase in the mammalian retina, identifying it as inhibitor or modulator of phosphorylation of retinal proteins.
At the level of mammalian heart tissue taurine is the most abundant amino acid and seems to be involved in the exchange of Na+ – Ca2+ in the heart.
In this regard, experimental and clinical studies on congestive heart failure have shown improvements and a reduction in mortality with specific treatments of taurine. In addition, other studies have shown that taurine may participate in the regulation of some of the cardiac proteins, including angiotensin II and pyruvate dehydrogenase.
Taurine is considered an essential amino acid during foetal growth and lactation, but there is no complete development of bioregulatory systems to maintain taurine at this stage, high concentrations of this amino acid were found in human breast milk and in the placenta.
Hypoglycemic effects of taurine have been reported both by some studies in 1930 and by others later in-depth and all reported that taurine boosts the effect of insulin. In fact, it has been found that diabetes and poorly controlled ketoacidosis are undoubtedly associated with high urinary excretion of taurine. Therefore in type 2 diabetic patients taurine has been suggested as a complementary therapeutic agent for diabetic complications.
In normal subjects the concentration of taurine at platelet level is very high. Studies have found that an increase of taurine and platelet glutathione in diabetics, improves the conditions of platelet aggregation which is one of the first symptoms of the disease.
Almost all diabetic patients, within about 20 years of the onset of the disease, develop retinal dysfunction in the form of retinopathy; and in most patients also develop problems of the nervous system, whose pathogenesis for the development of diabetic neuropathies is unknown. Studies in STZ-induced diabetic rats reported changes in taurine transport activities in diabetic neuropathy models and reduced absorption of taurine in the retina.
In diabetic patients, the development of reduced kidney function is common. Short-term studies in rats induced by STZ have shown a decrease in taurine in the kidney, while more in-depth studies have shown that the increase in taurine improves chronic diabetic nephropathy.
In diabetic diseases there is often a impaired neutrophilic function, which is more susceptible to infections. The altered immune system could be caused by an accumulation of sorbitol that depletes the taurine and therefore reduces the ability to defend. A study in hyperlipidemic rats showed that taurine could improve the reduced bactericidal capacity of neutrophils.
Mice of the C57BL/6 strain are predisposed to the development of atherosclerotic lesions, a fact that could be caused by decreased renal resorption of taurine and from the subsequent depletion. A further study of the same models reported a reduction in atherosclerotic lesions due to increases in taurine in the diet.
In conclusion, based on the information in this review, treatment with taurine and possibly other osmolites could be successful in preventing certain clinical complications typically observed in diabetes