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At least 19 recordsLinked to original sources
PubMed1991

Tissue taurine content, activity of taurine synthesis enzymes and conjugated bile acid composition of taurine-deprived and taurine-supplemented rhesus monkey infants at 6 and 12 mo of age.

Concentrations of taurine were measured in a number of tissues from rhesus monkeys fed a taurine-free human infant formula with or without taurine supplementation for 6 mo and 12 mo. At 6 mo, tissue taurine content was significantly greater in the monkeys supplemented with taurine, but by 12 mo, there was no longer a significant difference. Activities of enzymes involved in taurine biosynthesis did not differ between the groups at any age. There was no difference in biliary bile acid class composition between the groups, but the proportion of bile acids conjugated with taurine reflected the tissue taurine content (i.e., was significantly greater in monkeys supplemented with taurine at 6 mo). This difference also disappeared by 12 mo. These results indicate that dependence on dietary sources of taurine persists for at least the first 6 mo but declines by 12 mo. Thus, dietary taurine content is reflected in the tissue taurine content and proportion of bile acids conjugated with taurine in infant rhesus monkeys at least until 6 mo of age, but the body taurine status in animals 12 mo old or older is not an indicator of previous status.

Animal Nutritional Physiological Phenomena↗
PubMed1992

Urinary excretion of taurine as a function of taurine intake: potential for estimating taurine bioavailability in the adult cat.

Urinary taurine excretion increases markedly when excess taurine is consumed. Experiments were designed to characterize this response in an attempt to develop an assay system for taurine bioavailability in common cat foods using an adult cat model. Initial studies investigated the time course of changes in urinary taurine excretion in response to alterations in taurine intake. The rate of urinary taurine excretion decreased rapidly when cats were switched from a casein diet supplemented with 0.2% crystalline taurine to a diet containing no supplemental taurine, reaching steady-state in 2 d. In contrast, urinary taurine excretion by cats switched from low to high taurine did not plateau until 6 to 7 d. Subsequently, cats (n = 18) were fed a casein diet containing graded levels of crystalline taurine (0, 0.025, 0.05, 0.10, 0.15 or 0.20%). After a 7-d adjustment period, urinary taurine excretion was quantified over a 5-d collection period and also by cystocentesis, and blood taurine levels were measured on d 6. Plasma taurine increased linearly (r = 0.88) as taurine intake increased, while whole-blood taurine increased asymptotically, reaching 95% of maximum concentration at a taurine intake of 93 mu mole/(kg body weight.d). The rate of urinary taurine excretion increased only slightly as taurine intakes increased to 96 mu mol/(kg body weight.d), but increased markedly (15-fold) thereafter. The same pattern was observed whether urinary taurine excretion was expressed as mu mole/(kg body weight.d) from total urine collection or as mu mole/g creatinine from cystocentesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1978

Hepatic taurine concentration and dietary taurine as regulators of bile acid conjugation with taurine.

Taurine concentration in liver biopsies taken from 20 patients undergoing cholecystectomy or laparotomy for obstructive jaundice correlated with percentage of taurine-conjugated bile acids in hepatic bile. In biliary obstruction, taurine concentrations in muscle did not parallel high hepatic taurine concentrations, suggesting selective hepatic taurine accumulation in biliary obstruction. In fasting subjects with an intact bile acid enterohepatic circulation, per cent taurine-conjugated bile acids in bile was the same as per cent taurine conjugation of bile acids by the liver. Ingestion of small amounts of taurine (250 mg) can increase the per cent taurine conjugation by the liver. Of 10 subjects, 7 increased per cent taurine conjugation of bile acids by the liver by 2.5 to 10% at 2 1/2 hr after intraduodenal taurine administration. We conclude that hepatic taurine concentration is a major determinant of per cent taurine conjugation of bile acids by the liver in man. In the fasting subject with an intact enterohepatic circulation, per cent taurine-conjugated bile acid in the bile acid pool is very close to the per cent taurine conjugation of bile acids by the liver. Hepatic bile acid conjugation pattern may differ from that of the bile acid pool as a result of taurine ingested with meals, but the deviation is small, and acute alteration of the per cent taurine conjugation in the bile acid pool does not occur.

Bile↗
PubMed1978

Taurine deficiency in the kitten subcellular distribution of taurine and [35S]taurine in brain.

Taurine concentration decreases rapidly in the tissues and physiological fluids of kittens fed a diet of partially purified casein which lacks taurine. We have studied the subcellular distribution in cerebrum of taurine and [35S]taurine administered intravenously to these animals. The taurine concentration of all the fractions isolated from the cerebrum of taurine-deficient kittens was approximately sevenfold less than that observed in the fractions of cerebrum isolated from control kittens. The [35S]taurine was approximately twofold greater in all the brain fractions isolated from the taurine-deficient kittens compared with those isolated from the control kittens. The percent distributions of taurine and [35S]taurine in the fractions isolated from the cerebrum of control and deficient kittens were identical. Thus, in the face of a severe diet-induced deficiency of taurine in kitten brain, there appears to be no conservation of taurine by any particular subcellular pool of taurine. These studies provide no evidence for differences in compartmentation of taurine in cerebrum of taurine-deficient kittens compared with control kittens.

Animals↗
PubMed1991

Distribution of taurine-like immunoreactivity in cerebellum of kittens from taurine-supplemented and taurine-deficient mothers.

Using an antibody prepared against taurine conjugated to bovine serum albumin with glutaraldehyde, the distribution of taurine in cerebellum of newborn and 8-week-old kittens from mothers fed 0, 0.02, 0.05, or 1% dietary taurine has been determined. In general, taurine-like immunoreactivity was greater in kittens from mothers fed the greatest amounts of taurine, as was the total cerebellar taurine concentration. The most notable feature in newborn kitten cerebellum was a dense band of staining in the inner molecular layer adjacent to the Purkinje cell layer, which corresponds to the short Purkinje cell dendrites. In cerebellum of 8-week-old kittens, taurine-like immunoreactivity was present in Purkinje cells and their dendrites, most granule cells, and a few interneurons in the molecular layer of the 0.02, 0.05, and 1% groups. The cerebellum of the 0% group was distinctive in that virtually no neurons were reactive, appearing as 'ghosts' against the background, and both white matter and the granule cell layer contained large numbers of reactive astrocytes. The presence of such large numbers of reactive astrocytes and the immunoglobulin within the brain suggests an impairment of the blood-brain barrier in such taurine-deficient kittens.

Animals↗
PubMed1978

Taurine deficiency in the kitten: exchange and turnover of [35S] taurine in brain, retina, and other tissues.

Kittens fed a purified diet containing partially-purified casein as the source of protein become taurine-deficient and develop retinal degeneration. The present studies report the exchange and turnover of taurine in different areas of brain, retina and other tissues and fluids of control and taurine-deficient kittens. The various tissues and fluids have different rates of exchange and different half-lives of taurine; taurine deficiency causes a range of changes in these parameters. Generally, tissues and fluids from taurine-deficient kittens accumulated more [35S] taurine and had a longer half-life of taurine than tissues and fluids from control kittens. Nine areas of brain were studied and, of these areas, olfactory bulb had the greatest concentration of taurine. Olfactory bulb resisted taurine depletion to a greater extent than other areas; and, in contrast to other areas of brain, in taurine-deficient kittens, it accumulated [35S] taurine for most of the experiment. Retina resisted taurine depletion and, in taurine-deficient kittens but not in control kittens, it accumulated [35S] taurine throughout the experiment. The amount of taurine conjugated to bile acids was unchanged by the taurine depletion, but the kinetic behavior was altered and was similar to that of retina. The results provide support for the suggestion that, in the kitten at least, taurine is most important for the functions of bile and retina and that taurine depletion affects retina before bile. Taurine may have special importance in olfactory bulb but not necessarily in other regions of brain.

Adrenal Glands↗
PubMed1990

Effect of intravenous taurine supplementation on plasma, blood cell, and urine taurine concentrations in adults undergoing long-term parenteral nutrition.

Thirty-four adults undergoing long-term parenteral nutrition (TPN) were treated either with or without intravenous taurine for less than or equal to 24 mo. Statistical comparisons were carried out in eight patients randomly assigned to receive intravenous taurine, usually 10 mg.kg-1.d-1, and 10 patients not receiving taurine. Compared with normal adults, baseline plasma taurine and urine taurine-creatinine ratios were decreased in both groups and platelet taurine was reduced in the taurine-treated group. During taurine treatment the mean of the mean values for taurine became normal in plasma and platelets and remained normal in erythrocytes, granulocytes, and lymphocytes; urine taurine-creatinine ratios rose to approximately five times normal. During follow-up, patients not given taurine had plasma, erythrocyte, and granulocyte taurine and urine taurine-creatinine ratios below normal values and the concentrations of taurine-treated patients. Their platelet taurine was also subnormal. Thus, 10 mg taurine.kg-1.d-1 intravenously normalizes plasma and blood cell taurine concentrations in long-term TPN patients.

Adult↗
PubMed1987

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 result 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.

Animals↗
PubMed1992

Myocardial taurine concentrations in cats with cardiac disease and in healthy cats fed taurine-modified diets.

Myocardial taurine concentrations were measured in cats with cardiac disease and in healthy cats fed diets with various concentrations of taurine. Group 1 was composed of 26 cats with 3 categories of naturally developing cardiac disease: dilatative cardiomyopathy (group 1A), 10 cats; hypertrophic cardiomyopathy (group 1B), 9 cats; and volume overload (group 1C), 7 cats. These cats had been fed various commercial diets. Group 2 was composed of 40 healthy cats that had been fed diets varying in taurine concentration (0 to 1% taurine) for at least 2 years. Mean myocardial taurine concentrations did not differ significantly between group-1 cats with dilatative cardiomyopathy and those with hypertrophic cardiomyopathy or volume overload. Cats in group 1A had a mean myocardial taurine concentration 3 times higher than healthy cats fed a taurine-free diet (P less than 0.002). Mean myocardial taurine concentrations did not differ significantly between group-1A cats and healthy cats fed a diet containing 0.02% taurine; group-1A cats had significantly lower mean myocardial taurine concentrations than did healthy cats fed a synthetic diet containing 0.05 or 1.0% taurine (P less than 0.001). Acute oral administration of taurine in 5 group-1A cats appeared to increase mean myocardial taurine concentrations, compared with similar cats not given taurine during treatment for cardiac failure. In group-2 cats, mean myocardial taurine concentrations increased directly with percentage of dietary taurine.

Animals↗
PubMed1987

Is taurine a hypothalamic neurotransmitter?: A model of the differential uptake and compartmentalization of taurine by neuronal and glial cell particles from the rat hypothalamus.

Although taurine has been postulated to be a neurotransmitter or neuromodulator in the mammalian CNS, little is known concerning its role in brain function. Evidence suggesting that taurine may influence endocrine and homeostatic mechanisms via the hypothalamus resulted in our investigations into its function in this brain region. The main objectives of the research were to characterize the specific binding, uptake, and release of taurine in the hypothalamus. A specific aim was to examine the proposed neurotransmitter role for taurine in the hypothalamus. This was accomplished by comparing the characteristics and properties of the binding, uptake, and release of taurine with those for the classical neurotransmitters which satisfy the criteria for a neurotransmitter. On such a comparative basis, the characteristics of taurine uptake satisfy the neurotransmitter criterion of inactivation of taurine in the hypothalamus. However, the observed characteristics of taurine binding and release in the hypothalamus do not satisfy the respective neurotransmitter criteria of specific receptors and Ca2+-dependent evoked release. Therefore, solely on the basis of the experimental observations reported herein, we must conclude that taurine apparently does not function as a neurotransmitter in the hypothalamus. Two uptake systems were found in the P2 fraction, a high affinity uptake system and a low affinity uptake system. Uptake systems for taurine have previously been reported in glial and nerve cell homogenates, and therefore, because of the known contamination of crude synaptosomal preparations with glial particles, we sought to determine the cellular origin of the two taurine uptake systems in our crude preparation. Using a variety of diverse biochemical techniques such as hypo-osmotic shock, release experiments and Arrhenius plots, we determined that physical changes of the media or depolarizing stimuli which would influence neuronal and glial cell particles differently, also had differing effects on high and low affinity taurine uptake or its release from the respective uptake compartments. We conclude that the high affinity taurine uptake system/compartment is located on/in neuronal membranes/particles/particles and that the low affinity taurine uptake system/compartment is located on/in neuronal membranes/particles and that model for the differential cellular transport and compartmentalization of taurine into neuronal and glial cells has important implications concerning its possible role in the CNS.

Animals↗
PubMed1992

Urinary taurine excretion as a function of taurine intake in adult cats.

Experiments were designed to develop a urinary excretion model for the study of taurine status in adult cats. The time course of changes in urinary taurine excretion in response to alterations in dietary taurine was examined in Experiment 1. Urinary taurine excretion decreased rapidly when cats were switched from a casein diet supplemented with 2000 mg crystalline taurine/kg diet to a diet containing no supplemental taurine reaching a plateau in 2 d, but the cats required 7 d to reach a plateau when switched from the nonsupplemented diet to the 2000 mg taurine/kg diet. In Experiment 2, the casein diets contained graded levels of crystalline taurine (0, 250, 500, 1000, 1500 or 2000 mg/kg). After a 7-d adjustment period, urinary taurine excretion was quantified over 5 d, and blood taurine concentrations were measured on d 6. Plasma taurine concentration increased linearly (r = 0.88) as taurine intake increased, but whole-blood taurine increased asymptotically. Taurine intakes of greater than 96 mumol/(kg body wt.d) resulted in urinary excretion rates that were 15 times greater than those occurring below this break point. We suggest that urinary taurine excretion by cats fed taurine at levels above the break point has potential for estimating taurine bioavailability in intact meat-source proteins.

Animals↗
PubMed1986

Response of the kitten to dietary taurine depletion: effects on renal reabsorption, bile acid conjugation and activities of enzymes involved in taurine synthesis.

Kittens were adapted to a semipurified diet and then fed either a control diet that contained 0.1% taurine or a taurine-free diet for 6 weeks; at the end of the feeding period, kittens fed the taurine-free diet had plasma and liver taurine concentrations that were 0.38 and 0.15%, respectively, of those for control kittens. Hepatic cysteinesulfinate decarboxylase activity in taurine-deficient kittens was five-times the level in control kittens, but hepatic cysteine dioxygenase activity was not affected by the dietary treatment. Taurine-conjugated bile acids made up 98% of the total bile acids in the gall bladder of control kittens, but they accounted for only 44% of the total bile acids in the bile of taurine-depleted kittens; both the concentrations of taurine-conjugated bile acids and total bile acids were markedly decreased in taurine-deficient kittens. No effect of taurine depletion on the fractional excretion of taurine in the urine was observed. The kitten may have some mechanisms for adapting to a low-taurine diet, but these are clearly not sufficient to maintain tissue taurine levels in the absence of dietary taurine.

Animals↗
PubMed1992

The effect of dietary supplementation with cysteic acid on the plasma taurine concentration of cats maintained on a taurine-restricted diet.

The biochemical impairment in the taurine anabolic pathway of the cat has not yet been fully elucidated; however, a number of key enzymes are known to have reduced activity in the cat compared to the rat. There are a series of possible routes resulting in the formation of taurine, one of which is the decarboxylation of cysteic acid. The aim of this study was to investigate the effect of cysteic acid, as a precursor, on the circulating concentration of taurine. A group of twelve adult cats was fed a basal, canned diet containing 0.22 g taurine/kg fresh weight for a period of eighty-four days. The diet was supplemented with 2.0 g/kg fresh weight L-cysteic acid on day fifteen through fifty six and plasma taurine concentration was measured every two weeks throughout the study. The results showed that when the dietary intake of taurine was inadequate to maintain the plasma concentration above 40 mumol/L, the addition of L-cysteic acid to the diet gave rise to an increase in plasma taurine concentration in some cats. Eight of the twelve cats showed a significant rise in plasma taurine after dietary supplementation for six weeks (52.0 +/- 22.3 vs 212.4 +/- 97.9 mumol/L, p less than 0.01) and a subsequent decrease in plasma levels when the cysteic acid was withdrawn (65.6 +/- 37.1 mumol/L). The other four cats showed no significant rise in plasma taurine after six weeks supplementation (13.5 +/- 4.2 vs 35.5 +/- 19.4 mumol/L, ns). However, withdrawal of the cysteic acid resulted in a subsequent decrease in circulating levels of taurine (11.8 +/- 1.5 mumol/L, ns). These data indicate that the addition of cysteic acid to a taurine-restricted, canned diet will, in some cats, result in the biosynthesis of taurine. The plasma taurine concentration of the remaining cats, although not apparently increasing significantly, was maintained at a slightly higher constant level until the cysteic acid was withdrawn. These results suggest that cats are able to synthesise taurine via an alternative pathway utilising L-cysteic acid as a precursor, although the efficiency of this process differs considerably among individual animals.

Animal Nutritional Physiological Phenomena↗
PubMed1992

High dietary taurine effects on feline tissue taurine concentrations and reproductive performance.

The reproductive performance and outcome of kittens was determined for female cats fed 0.05, 0.2 or 1% taurine. No adverse effects of high taurine diets were noted in the adults or offspring, and the reproductive performance was slightly better than that of females fed the normal (0.05% taurine) diet. Body weight at birth and brain weight at weaning were significantly greater in the very high taurine group than in the normal taurine group, although the greatest growth rate was achieved by the normal taurine group. The concentration of taurine in milk of lactating females was substantially higher in cats fed the higher taurine diets. Brain of adult cats was resistant to increases in brain taurine concentrations, as was brain of newborn cats. However, brain of juvenile cats responded to higher dietary taurine intake with increased taurine concentrations. These results indicate that the higher taurine content in cat foods recently introduced for prevention of feline dilated cardiomyopathy should have no adverse effects over a prolonged period on health and reproduction of cats.

Administration, Oral↗
PubMed1992

Beneficial effect of intravenous taurine infusion on electroretinographic disorder in taurine deficient rats.

We investigated the effect of intravenous taurine infusion on the electroretinogram (ERG) of taurine-deficient rats produced by treatment with guanidinoethyl sulfonate (GES), a taurine transport inhibitor. Mother rats were fed a taurine-free diet and given drinking water containing 1% GES from 2 weeks of gestation to weaning. The same feeding conditions were applied to male offspring after weaning. Both ERG measurement and continuous infusion of taurine at a dose of 10, 30 or 100 mg/animal/day were performed for 3 weeks from 7 to 10 weeks of age. GES-treatment reduced a- and b-wave amplitudes to 50% of the control levels and also increased b-wave latencies. Intravenous infusion of taurine improved these ERG abnormalities in a dose-dependent manner. Taurine concentrations in plasma, eyes and brain were also decreased by treatment with GES, and dose-dependent recovery was observed after infusion with taurine, although the concentrations of other amino acids were not affected by GES-treatment and infusion of taurine. Observations of morphological changes revealed that the retinal damage in GES-treated animals was decreased by taurine infusion. These results indicate that the changes in ERG and retinal structure observed in taurine deficiency are improved by intravenous infusion of taurine.

Amino Acids↗
PubMed1977

Taurine in developing rat brain: transfer of [35S] taurine to pups via the milk.

The concentration of taurine in rat milk is very high for the first few days after birth and then falls rapidly. [35S]Taurine injected intraperitoneally into lactating dams after birth was transferred via the milk to the pups, and accumulated in the brains of the pups to a greater extext than in the livers of the pups. Maximal accumulation of [35S]taurine so transferred to the brain of the pups was reached by 5 days after birth, and remained constant for at least 10 days beyond this poiht. The specific radioactivity in the brain of the pups also reached a maximal value at 5 days after birth and thereafter declined because of the expanding pool of unlabeled taurine in brain. At 5 days after birth, each pup has received approximately 4 mumol taurine from the mother via the milk, and a minimum of 7% of the total taurine in brain at this time originated from the milk. Speculation Even in the rat, a species which can synthesize taurine very easily from cysteine and methionine precursors, a significant amount of performed taurine is transferred to the developing animal via the milk. We suggest that the human infant, who cannot synthesize adequate taurine from cysteine and methionine precursors (9, 10, 40), may be dependent on its diet as a taurine source. Human milk contains a high concentration of taurine, whereas synthetic formulas contain virtually none. Taurine may be an essential nutrient for the rapidly growing human infant (and may be for the adult human also) and perhaps should be included as a supplement in synthetic formulas.

Animals↗
PubMed1987

Taurine and GABA release from mouse cerebral cortex slices: potassium stimulation releases more taurine than GABA from developing brain.

The release of exogenous taurine and gamma-aminobutyric acid (GABA) was studied with slices from the developing mouse cerebral cortex. The spontaneous efflux of GABA increased with the cerebral GABA content during postnatal development, while the spontaneous efflux of taurine was approximately the same in both neonate and adult mice, in spite of a several-fold higher cerebral taurine content in the former. GABA, taurine and their structural analogues caused marked homo- and hetero-trans-stimulation of the release in both adult and developing mice, probably via membrane transport sites. The release was greatly enhanced by both 0.01 mM veratridine and exposure to sodium-free medium, the effects being more pronounced with GABA in the adults and with taurine in the neonates. The excitatory amino acids homocysteate, aspartate and kainate enhanced taurine release particularly from the developing cerebral cortex but were not effective on GABA release in the adults. The potassium stimulation of taurine release had a strikingly slow time course in both adult and developing mice. The responses in GABA release were also fairly slow in the neonates. Potassium stimulation evoked a large release of GABA in adult but not in developing mice. The evoked taurine release was in developing mice several-fold greater than the evoked GABA release, decreasing in magnitude with age. The potassium-stimulated release was only partially calcium dependent, more so with GABA in the adults and with taurine in the neonates, but a high magnesium ion concentration inhibited the release of both amino acids more strongly in the latter age group. Verapamil (0.1 mM) almost abolished the potassium stimulation of GABA release in both adult and neonate mice and was more effective on taurine release in neonate mice. The results suggest that taurine, not GABA, is the major inhibitor of excitability in developing mouse brain.

Aging↗
PubMed1989

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.

Adaptation, Biological↗