Taurine Intake Research Articles

Effect of Dietary Taurine on Renal Taurine Transport by Proximal Tubule Brush Border Membrane Vesicles in the Kitten

Renal adaptation of the kitten to altered dietary taurine intake was assessed using proximal tubule brush border membrane (BBM) vesicles. Three groups of kittens were adapted to purified diets containing 43.5% soy protein that were either taurine-free (OT) or contained 0.15% taurine (NT) or 1.0% taurine (HT). The plasma taurine concentration of the kittens fed OT decreased from 104 +/- 25 microM to 16 +/- 5 microM and 1.7 +/- 0.5 microM in 1 and 6 wk, respectively. Feeding HT increased plasma taurine concentration to 350 +/- 116 microM in 1 wk. Compared to NT, taurine accumulation by BBM vesicles was significantly elevated after 4 wk of feeding OT and decreased after 2 wk or less of feeding HT (P less than 0.05). Maximum renal adaptation occurred by 6 wk of feeding OT (206% increase in taurine uptake/15 s compared to NT) and by 2 wk or less of feeding HT (43% decrease in taurine uptake/15 s compared to NT). Evaluation of transport kinetics using renal cortex from groups of four kittens (16 determinations) fed NT, OT (12 wk) or HT (10 wk) revealed a Vmax of 55 +/- 10, 123 +/- 24 or 39 +/- 7 pmol.mg protein-1.10 s-1 and a Km of 32 +/- 7, 16 +/- 2 or 37 +/- 8 microM, respectively. The differences in Vmax and Km were significant between NT and OT (P less than 0.05), but not significant between NT and HT (P greater than 0.05). Our results suggest that renal adaptation of the kitten to changes in dietary taurine occurs with modifications of both Vmax and Km of the taurine transport system.

Plasma and muscle free amino acids during continuous ambulatory peritoneal dialysis

Free amino acids (AA) were determined in plasma and in muscle tissue of 29 patients undergoing continuous ambulatory peritoneal dialysis (CAPD) for 2 to 38 months. Muscle biopsies were taken in the morning after an overnight dwell with 1.36% glucose dialysis fluid. Muscle intracellular water was calculated using the chloride method. The intracellular (ic) and extracellular (ec) concentration and the ic/ec gradient for each AA was calculated and compared with values in matched healthy controls. Most of the essential and several non-essential AA were low in plasma. By contrast, none of the essential AA were low in muscle, and methionine was increased as were ornithine, asparagine, and aspartic acid; however, muscle taurine was markedly reduced. The ic/ec gradient was increased for most essential and several non-essential AA. In plasma, taurine precursors, methionine and cysteine, were not reduced and the ratios taurine/cysteine and taurine/methionine were low. Muscle taurine/methionine was also low. Thus, during CAPD muscle free AA are, in general, well maintained, suggesting that marked reductions of plasma AA levels in CAPD patients may reflect an ec to ic shift rather than depletion. The finding of low muscle taurine, but normal or increased cysteine and methionine pools, suggests that taurine depletion during CAPD is caused by blocked synthesis or low intake of taurine.

Randomized Trial of Taurine Supplementation for Infants \g=le\1,300-Gram Birth Weight: Effect on Auditory Brainstem-Evoked Responses

Taurine may be important to the developing eye and brain of the small preterm infant. A blinded randomized trial was conducted to determine whether taurine supplementation of healthy infants of \g=le\1,300 g birth weight until their discharge from the hospital increases their growth rate, neurobehavioral development, electroretinographic development, or maturation of auditory brainstem-evoked responses. Infants were fed with Similac Special Care as desired, which was prepared to contain < 5 mg/L of taurine or 45 mg/L of taurine, a concentration similar to that of human milk. Infants who did not receive taurine supplementation (n = 19) and those who did (n = 18) were similar with respect to condition at study entry, caloric intake, and growth rates throughout the study, and electroretinographic findings and scores on the Brazelton Behavioral Assessment Scale at 37 weeks' postmenstrual age. Infants who received taurine supplementation had greater overall plasma taurine concentrations. The group receiving taurine supplementation also had more mature auditory-evoked responses at 37 weeks' postmenstrual age with a modest (0.2 to 0.5 ms) but consistent reduction (P < .05) in the interval between stimulus and response at two different stimulation rates. Although further study is needed, taurine intake appears to influence auditory system maturation of preterm infants.

Effect of taurine administration on serum lipid and biliary lipid composition in man.

The effect of oral administration of taurine (3.2 g/day, 2 weeks) on the metabolism of lipids and bile acids was studied with healthy humans. Four male subjects were fed taurine. Another five male subjects were administered 1 g of cholesterol daily for two weeks and, at intervals of two weeks, cholesterol and taurine simultaneously. Serum lipoprotein and duodenal bile were analyzed. Oral administration of taurine resulted in the increase of taurine-conjugated bile acids. However, neither serum lipid nor biliary lipid composition was altered. Addition of taurine with cholesterol administration showed elevation of both the serum low density lipoprotein cholesterol level and the lithogenic index in bile. The ratio of glycine-to taurine-conjugated bile acids was changed from 4.1 to 0.63. The ratio of cholic acid/chenodeoxycholic acid was augmented from 0.57 to 0.81. The percentage of taurocholic acid, taurochenodexycholic acid and taurodeoxycholic acid were increased about 4-fold, 2.5-fold and 3-fold, respectively. Our results suggested that taurine administration alone did not influence the serum lipid level although taurine-conjugated bile acids were increased. The taurine intake would increase serum low density lipoprotein cholesterol and biliary cholesterol levels when excessive cholesterol is administered simultaneously.

Taurine in Development

Taurine is a ubiquitous dietary constituent of most mammals and is present in especially high concentrations in the tissues of developing mammals. Research to date indicates that taurine plays an important role in the development of the nervous system and the process of migration in particular. It is speculated that taurine uptake and release, in conjunction with glutamate uptake and release, may represent one form of communication between neurons and glial cells. The need of taurine by the body is emphasized by the ability of the kidney to curtail taurine excretion to conserve taurine in the face of a low dietary taurine intake. The evidence for a special role of taurine in development is considered and discussed.

Plasma and urine taurine levels in vegans

Plasma taurine levels and urinary taurine excretion were measured in 12 strict vegetarian (vegan) males who had maintained a vegan diet for 53 +/- 26 mo (SD) and in 14 male nonvegetarian control subjects. Plasma taurine levels differed (45 +/- 7 vs 58 +/- 16 mumol/L, respectively). Urinary taurine excretion was lower (266 +/- 279 vs 903 +/- 580 mumol/d), urinary N pi-methylhistidine was barely detectable, and urinary N tau-methylhistidine was significantly reduced (296 +/- 87 vs 427 +/- 19 mumol/d) in the vegans. Analysis of 3-d dietary diaries kept by the vegans indicated marginal to adequate intake of protein, carbohydrate, vitamin B-6, methionine, and cystine; inadequate intake of zinc; and negligible intake of taurine. Prolonged absence of dietary taurine intake causes decreased plasma taurine and severely restricted urinary taurine output.

Excessive fecal taurine loss predisposes to taurine deficiency in cystic fibrosis.

Elevation of the ratio of glycine: taurine-conjugated bile acids (G/T ratio) is thought to contribute to fat malabsorption in cystic fibrosis (CF). The cause, extent, and reversibility of taurine deficiency in CF were assessed using balance studies in 6 subjects (ages 8-14 years) who were supplemented with taurine (0.24-2.4 mmol/kg/24 h) for 1 week. Taurine reduced the G/T ratio both in serum and duodenal juice in all children. The mean fecal taurine loss in CF subjects [10.8 mumol/kg/24 h +/- 9.9 (SD), range 0.9-27.9] was much greater than that in controls (less than 0.1 mumol/kg/24 h, n = 4) and approximated the dietary taurine intake (mean 14.6 +/- 4.4 mumol/kg/24 h, n = 12). Absorption of an oral taurine load appeared to be normal in CF. Excessive fecal taurine loss appears to predispose CF children to bile acid taurine deficiency, a deficiency that can be corrected by oral taurine supplements.

Effect of Dietary Taurine on Plasma and Blood Cell Taurine Concentrations in Cats

Taurine levels were measured in adult cats consuming casein-based diets supplemented with 0.2, 0.05, 0.02, 0.01 or 0% (wt/wt) taurine or with 0% taurine plus 5.0% L-cystine. Taurine concentrations in plasma, platelets, granulocytes and erythrocytes declined significantly with decreased dietary taurine. In the cats that did not receive the 5.0% cystine supplement, the relationship between dietary taurine intake and plasma and blood cell taurine level was nonlinear. The greatest increment in taurine concentrations occurred between the 0.02 and 0.05% taurine intakes. These findings suggest that the dietary taurine requirement for adult cats may be between 0.02 and 0.05%. Supplementation of the 0% taurine diet with 5.0% L-cystine raised taurine levels above those of the taurine-deficient diets in plasma and all blood cell types. The results of this study therefore suggest a close relationship between dietary taurine intake and blood cell taurine levels in cats. Five percent L-cystine stimulates taurine synthesis in these animals.

Effects of high dietary methionine on activities of selected enzymes in the liver of kittens ( felis domesticus)

1. 1. Growing male kittens were fed an 18% casein diet supplemented with 2, 3, or 4% l-methionine (MET) for 6 weeks. 2. 2. Free MET concentration in liver increased 30-fold and cystathionine two- to three-fold; the activity of adenosyl-MET transferase and cystathionase also increased but remained lower than previously found in rats. 3. 3. Taurine concentration in liver decreased in cats fed excess MET and appeared to depend on taurine intake. 4. 4. Alanine aminotransferase activity was high in all groups while serine dehydratase activity was very low. 5. 5. Pyruvate kinase and malic enzyme activities which are normally low in cat liver increased after excess MET. Also, glucose 6-phosphate and 6-phosphogluconate dehydrogenases increased. 6. 6. Cat liver metabolism showed limited adaptation to an excess dietary intake of methionine compared to that found in rats.

Taurine concentrations in plasma and blood cells of patients undergoing long-term parenteral nutrition

Taurine concentrations were measured in plasma and blood cells of 40 adults undergoing long-term parenteral nutrition, without intravenous taurine, for 43.8 ± 35.1 (SD) mo. Patients were classified into Group 1 (21 patients) or Group 2 (19 patients) according to whether their estimated enteral absorption of calories was less or greater than 25% of their daily requirement, respectively. In Group 1, taurine concentrations were reduced to 35–49% of normal control values in plasma (p < 0.01), platelets (p < 0.001), lymphocytes (p < 0.005), and erythrocytes (p < 0.001). Granulocyte taurine was not different from normal. A smaller decrease in taurine concentration was found in Group 2 patients; however, taurine levels were significantly below normal in their plasma and red cells. Thus, many patients undergoing long-term parenteral nutrition with little or no taurine intake are depleted of taurine in plasma and most blood cells. These findings suggest that taurine may be essential for these patients and should be added to solutions used for long-term parenteral nutrition.

Metabolic effects of a human milk adapted formula on sulfur amino acid degradation in full-term infants.

The metabolic effects of formula feeding on sulfur amino acid degradation were studied in 6 full-term infants on the 6th day of life, and compared to corresponding data from breast-milk fed neonates. A normal excretion of total sulfur and inorganic sulfate was found, indicating an adequate intake of sulfur amino acids and a normal ability to oxidized these compounds to inorganic sulfate. A similar transaminative degradation of cysteine was observed in both groups. Formula-fed infants showed a normal output of methionine, whereas increased cystathionine and decreased taurine excretions were registered. The results were probably a combined effect of a limited intake of taurine, and a multiple immature enzymatic activity.

Taurine deficiency in the developing cat: persistence of the cerebellar external granule cell layer.

Dietary taurine deprivation adversely affects feline pregnancy and is associated with the frequent occurrence of fetal resorption, abortion, stillbirth, and low birthweight of live kittens at term. Taurine-deprived, live-born kittens have a poor postnatal survival rate and grow less well than kittens from taurine-supplemented queens. The postnatal dietary taurine intake of such kittens is reduced if they are nursed by their biologic mothers; the concentration of taurine in milk of taurine-deprived mothers is less than 10% of that in milk from taurine-supplemented queens. Surviving kittens from taurine-deprived mothers exhibit a constellation of neurological abnormalities (abnormal hind leg development, a peculiar gait characterized by excessive abduction and paresis, and thoracic kyphosis readily visible by X-ray). These findings suggest the presence of a developmental cerebellar deficit. Histological examination of the pre- and postnatally taurine-deprived kitten's cerebellum reveals a persistence of the external granule cell layer, which was confirmed by electron-microscopic examination. Numerous mitotic figures are present in the cells in the external granule cell layer of the cerebellum of kittens born from the nursed by taurine-deprived queens, but not in those from taurine-supplemented mothers. These findings suggest a maturational delay.

Renal adaptation to alteration in dietary amino acid intake.

The nonessential beta-amino acid taurine, which is inert in renal tissue, was used to study the renal adaptation to dietary taurine change. Three isoproteinic diets were employed: HTD--high in taurine, NTD--normal taurine, and LTD--deficient in the taurine precursors cysteine and methionine. When compared with NTD, HTD resulted in an increase in the urinary excretion and fractional excretion of taurine, whereas LTD led to a decrease in urinary excretion and fractional excretion of taurine. In vitro studies demonstrated an increase in the Vmax of the high-affinity, low-capacity uptake system with no change in "apparent" Km following LTD. Complete adaptation developed within days after the diet was changed (NTD to HTD = 3 days; NTD to LTD = 3-6 days). These studies demonstrate that the renal response to altered dietary amino acid can be evaluated and that adaptation occurs for the beta-amino acid taurine. The renal response serves to conserve taurine during periods of deprivation and to dispose of taurine during periods of excess. The renal adaptation to restricted taurine intake seems to occur through an increase in transport sites (increased Vmax) or change in flux at the transport sites, with no change in transport affinity (unaltered apparent Km).

The taurine requirement of the adult cat

ABSTRACTThe taurine requirement of adult cats was investigated using a purified amino‐acid diet containing various levels of added taurine. From the results of two earlier investigations it appeared that the minimum daily taurine requirement was between 35 and 56 mg for an adult cat. The results of the present study show that a taurine intake of about 10 mg/kg bodyweight/day is sufficient to maintain adult cats in adequate taurine status. This value is in agreement with the previous estimate and approximates to a taurine concentration of 500 mg/kg of dry matter in a commercial cat food.

Effect of taurine supplementation to the diet on bile acid conjugation in low birth-weight infants (LBWI): 74

Previous results have shown that plasma and urine taurine concentrations decrease when LBWI are fed with taurine deficient formulas. In this study, 63 well LBWI with gestational ages of 31 to 36 weeks were randomly assigned to either breast milk (BM) or formula (1.5%, prot. 60:40 whey: caseins) without (F1) or with addition of taurine (30 μmol%, F2). Duodenal fluid bile acids and glycine-taurine ratio (G:T) were determined with high-performance liquid chromatography. The plasma taurine levels and urine taurine excretion fell significantly in the infants fed with the taurine deficient F1 formula. At the age of 7 days the G:T ratios were 0.64 (BM), 0.44 (F1) and 0.47 (F2). In the infants on BM and F2 the G:T ratio remained on the same level throughout the study and at the age of 36 to 40 days it was 0.58 and 0.69 respectively on the two diets. In the infants fed with formula F1, the G:T ratio increased significantly after the age of 21 days being 1.32 at a mean age of 39 days (p<0.001). Our results indicate that dietary taurine intake affects duodenal bile acid conjugation.

Dietary-Induced Variations in Urinary Taurine Levels of College Women

Dietary-induced variations in the urinary taurine excretion of healthy college women were investigated. Data were collected in three metabolic studies in which nutritionally adequate diets of constant composition were fed. Variables included isonitrogenous natural food and semi-purified diets; taurine, cystine and meat supplements; and kind and amount of dietary fat. Observed urinary taurine levels were low and ranges were narrower than those reported by other investigators. The low taurine excretion at the completion of the studies was considered evidence that urinary taurine levels in humans is related to the level of body taurine as well as to the level of dietary taurine. Urinary taurine excretion was shown to be related to dietary taurine intake rather than protein (nitrogen) intake. A relationship between kind of dietary fat and taurine excretion is suggested.

The connective tissue apparatus of the orbit

<dm:abstracts xmlns:dm="http://www.elsevier.com/xml/dm/dtd"><ce:abstract xmlns:ce="http://www.elsevier.com/xml/common/dtd" view="all" class="author" id="aep-abstract-id1"><ce:section-title>Publisher Summary</ce:section-title><ce:abstract-sec view="all" id="aep-abstract-sec-id1"><ce:simple-para id="fsabs056" view="all">The ampholytic amino acid taurine is a conditionally essential nutrient. It plays a critical role in kidney function and protection of cells against dehydration, eye and brain function, hormonal regulation, nutrient absorption (bile), and protection against oxygen free radicals (hypotaurine). Clams, fish, and meat are the best sources, and human milk is a good source for infants. Taurine is absent from a lacto-ovo-vegetarian or vegan diet. A lack of taurine in young infants may cause irreversible degeneration of the retina, limit brain maturation, and slow growth and weight gain. The risks from very high taurine intakes (&gt; 1-2 g/day) are not known. Significant amounts of taurine are secreted with bile as conjugates with bile acids, which are cleaved by bacterial henodeoxycholoyltaurine hydrolase. Free taurine is taken up from the small intestinal (ileal) lumen by a sodium chloride-dependent cotransporter. The GABA transporter I is expressed in small intestine and might be solely or in part responsible for this transport activity. Taurine is transported out of the enterocytes by the NaCl-dependent taurine transporter. Normally about 2–3% of excreted bile acids is lost with feces and the attached taurine with them. Daily taurine losses may be estimated at 60 mg assuming total bile acid losses of 500 mg, about half of which will be conjugated with taurine.</ce:simple-para></ce:abstract-sec></ce:abstract></dm:abstracts>

Metabolism of [35S]Taurine in Man

Taurine metabolism in man was defined by an isotope dilution technique during normal taurine intake (five subjects) or increased taurine intake (two subjects). A tracer dose of [35S]taurine was administered intravenously, and the amount and chemical form of radioactivity were determined in blood, urine, bile, and feces. Analysis of plasma specific activity decay curves indicated that taurine metabolism can be described by two exchangeable pools: a small (2 mmoles), rapidly exchanging pool (t1/2 approximately equal to 0.1 hour); and a large (98 mmoles), very slowly exchanging pool (t1/2 approximately equal to 70 hours). A small amount of [35S]isethionic acid was detected in urine, possibly the result of deamination of taurine by tissues; but otherwise no evidence of tissue biotransformation was obtained. Taurine was excreted predominantly (95%) in urine, about 70% as taurine and 25% as sulfate. The sulfate was considered to be formed in the intestine by bacterial degradation of taurine and then absorbed. Supplemental taurine (given orally) was well absorbed, caused a transient increase in plasma taurine levels, was excreted in urine without equilibration with the slowly exchangeable pool, and caused only a modest increase in total body taurine. Thus, taurine resembles other amino acids in having large tissue pools but differs strikingly in being metabolically inert with an extremely slow turnover rate.

Effect of Catalin ® (1-hydroxy-(3,2α)-5-phenoxazone-3-carboxylic acid) on the reduced coenzymes NADH and NADPH

Taurine is a small sulfur amino acid found in high amounts in mammalian eyes and is the most abundant amino acid in the retina. Although taurine can be synthesized endogenously, the main source is the diet. This exogenous taurine intake is regulated by active taurine uptake into tissues by a specific taurine transporter. Taurine depletion, by administering a taurine-free diet or selective blocker of the taurine transporter, generates severe retinal damage in the photoreceptor layer. Taurine depletion has been implicated in the retinal toxicity of the antiepileptic drug vigabatrin, characterized by cone damage and loss of retinal ganglion cells (RGCs). The taurine dependency for RGC survival was further demonstrated on purified RGC cultures and animal models of RGC degeneration. Reduced retinal blood perfusion may lead to decreased retinal taurine uptake from the blood and to RGC loss. High levels of taurine are present in the anterior part of the eye. Taurine may prevent the development of cataract and dry eye through its osmoregulatory action. Taurine dietary intake is therefore a major factor in eye health.