There is no evidence that inositol is a dietary essential, because it is synthesized by all eukaryotic cells. Infants may have a higher requirement than can be met by endogenous synthesis, and dietary inositol is a growth factor for the newborn mouse. In female gerbils, inositol is a dietary essential, and deficiency
leads to lipodystrophy, mainly as a result of impaired synthesis and secretion of plasma lipoproteins.
People with untreated diabetes have high plasma concentrations of free inositol, and high urinary excretion of inositol, associated with relatively low intracellular concentrations of inositol, suggesting that elevated plasma glucose may inhibit the uptake of inositol. There is some evidence that impaired nerve conduction velocity in diabetic neuropathy is associated with low in-tracellular concentrations of inositol and that inositol supplements improve nerve conduction velocity. However, high intracellular concentrations of in-ositol also impair nerve conduction velocity, and supplements may have a deleterious effect.
Taurine was discovered in 1827 in ox bile, where it is conjugated with the bile acids. It was later shown to be a major excretory product of the sulfur amino acids methionine and cysteine. Until about 1976, it was assumed that it was a metabolic end-product whose only function was the conjugation of bile acids. In the rat, taurine synthesis accounts for 70% to 85% of total cysteine catabolism.
Kittens fed on diets with little preformed taurine develop retinal degeneration and blindness, which is prevented by taurine supplements. In the early stages, electroretinography shows changes similar to those seen in human retinitis pigmentosa. However, there is no evidence that retinitis pigmentosa is associated with taurine deficiency, and patients have normal plasma concentrations of the amino acid. Electron microscopy of the retinae of deficient kittens shows early disorientation of the cone photoreceptor outer segments, followed by extensive degeneration of both rod and cone outer segments. Children maintained on long-term total parenteral nutrition without added taurine show changes in the electrical activity of the retina, suggesting that endogenous synthesis may be inadequate to meet requirements. The function of taurine in the retina (and possibly other tissues) seems to be mainly as an osmolyte, maintaining normal intracellular osmolarity.
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