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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↗
PubMed1996

Nitric oxide-evoked [3H]taurine release is mediated by reversal of the Na(+)-dependent carrier-mediated taurine transport system.

The pharmacological characteristics of [3H]taurine release evoked by nitric oxide (NO) were investigated using mouse cerebral cortical neurons in primary culture. N-Methyl-D-aspartate (NMDA) and S-nitroso-N-acetylpenicillamine (SNAP) dose-dependently increased [3H]taurine release from neurons. The NMDA-evoked release of [3H]taurine was reduced to the basal level by N omega-nitro-L-arginine, a NO synthase inhibitor, and MK-801, a noncompetitive antagonist for NMDA receptors. The NMDA- and SNAP-evoked releases of [3H]taurine were completely abolished by hemoglobin, indicating that these [3H]taurine releases were evoked by NO produced by NMDA receptor activation and liberated from SNAP. Withdrawal of Na+ from incubation buffer significantly inhibited the NMDA- and SNAP-induced [3H]taurine releases, whereas removal of Ca2+ produced no alteration in the SNAP-evoked [3H]taurine release. In addition, beta-alanine and guanidinoethane sulfonate, antitransporters of the carrier-mediated taurine transport system, reduced the NMDA- and SNAP-evoked releases of [3H]taurine in a dose-dependent manner. These results indicate that the NO-evoked [3H]taurine release from cerebral cortical neurons is mediated by a reversal of the Na(+)-dependent carrier-mediated taurine transport system.

Animals↗
PubMed1994

Effects of taurine and taurine analogues on the phosphorylation of a 44 kDa protein present in a mitochondrial subfraction of the rat heart: partial characterization of the 44 kDa phosphoprotein.

Recent studies suggest that taurine (2-aminoethanesulfonic acid) is involved in the regulation of protein phosphorylation in excitable tissues such as the retina, brain and heart. In order to determine the structural requirements for the effect of taurine on the phosphorylation of a 44 kDa protein(s), a series of taurine analogues were tested in an in vitro assay using a subcellular mitochondrial fraction of rat heart. Inhibitors of the phosphorylation of the 44 kDa protein include taurine and close structural analogues of taurine such as aminoethylhydrogen sulfate and alpha-sulfo-beta-alanine. Secondary amines with the taurine structure partially locked into a saturated 5-membered ring such as (+/-)piperidine-3-sulfonic acid and 1,2,3,4-tetrahydroquinoline-8-sulfonic acid also possess inhibitory activity. Sulfone analogues of taurine such as 2-aminoethylmethylsulfone, a non-restricted taurine analogue with maximal conformational flexibility about its amino and sulfone moieties, and (+/-)3-aminotetrahydrothiopyran-1,1-dioxide, an analogue containing the sulfone moiety in a six-membered ring structure, were found to be more potent inhibitors of phosphorylation than taurine despite the fact that the sulfone moiety is neither an isosteric nor isoelectronic substitution for the sulfonic acid moiety. The results of this study indicate that the inhibition of the phosphorylation of the 44 kDa protein in a rat heart mitochondrial fraction is relatively specific for the taurine structure. Two analogues of taurine with unsaturated rings containing a primary sulfonic acid and a secondary amine, pyridine-3-sulfonic acid and quinoline-8-sulfonic acid, were observed to be stimulators of the phosphorylation of the 44 kDa protein. In addition, 2-aminobenzenesulfonic acid also stimulated phosphorylation. Phase separation experiments with Triton X-114 suggest that the 44 kDa phosphoprotein is a soluble protein and not an integral membrane protein of the mitochondria. Phosphate incorporation into specific amino acids was determined by two-dimensional electrophoresis on celluloses plates and was found exclusively in the serine residues.

Animals↗
PubMed2003

The effects of systemically administered taurine and N-pivaloyltaurine on striatal extracellular dopamine and taurine in freely moving rats.

The second most abundant cerebral amino acid, taurine, is widely consumed in the so-called "energy drinks". Therefore, its possible actions on the brain are of great interest. In the present experiments taurine was given intraperitoneally to rats in order to study if it can be administered systemically in large enough amounts to alter cerebral dopaminergic transmission or to induce hypothermia. In addition, the effects of subcutaneously administered lipophilic taurine analogue, N-pivaloyltaurine, were studied. The extracellular striatal taurine and dopamine concentrations were estimated using in vivo microdialysis in awake and freely moving rats, and the rectal temperatures were measured. Taurine at the total dose of 45 mmol/kg i.p. led to a maximally 8-fold increased striatal extracellular taurine concentration, induced a long-lasting hypothermia, and significantly reduced the striatal extracellular dopamine concentration. The latter effect was strengthened by co-treatment with reuptake inhibitor nomifensine. N-pivaloyltaurine (15 mmol/kg in total, s.c.) only slightly elevated the striatal extracellular taurine concentration, failed to alter the rectal temperature, and in contrast to taurine somewhat elevated the striatal extracellular dopamine concentration suggesting a different mechanism or locus of action from that of taurine. Finally, our experiments using brain microdialysis confirmed the earlier findings that taurine is slowly eliminated from the brain. The results clearly indicate that systemically given taurine enters the brain in concentrations that induce pharmacological effects.

3,4-Dihydroxyphenylacetic Acid↗
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↗
PubMed2003

A specific taurine recognition site in the rabbit brain is responsible for taurine effects on thermoregulation.

(1) Taurine and GABA are recognized as endogenous cryogens. In a previous study, some structural analogues of taurine, namely 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and (+/-)cis-2-aminocyclohexane sulfonic acids (CAHS) have been shown to displace [(3)H]taurine binding from rabbit brain synaptic membrane preparations, without interacting either with GABA-ergic systems, nor with taurine uptake mechanism, thus behaving like direct taurinergic agents. (2) To answer the question whether the role of taurine as an endogenous cryogen depends on the activation of GABA receptors or that of specific taurine receptor(s), taurine or the above structural analogues were injected intracerebroventricularly in conscious, restrained rabbits singularly or in combination and their effects on rectal (RT)- and ear-skin temperature and gross motor behavior (GMB) were monitored. (3) Taurine (1.2 x 10(-6)-4.8 x 10(-5) mol) induced a dose-related hypothermia, vasodilation at ear vascular bed and inhibition of GMB. CAHS, at the highest dose tested (4.8 x 10(-5) mol) induced a taurine-like effect either on RT or GMB. On the contrary ISE, injected at the same doses of taurine, induced a dose-related hyperthermia, vasoconstriction and excitation of GMB. AEA and TAG caused a dose-related hyperthermia, but at doses higher than 1.2 x 10(-7) mol caused death within 24 h after treatment. (4) CAHS (4.8 x 10(-5) mol) antagonized the hyperthermic effect induced by TAG (1.2 x 10(-6) mol), AEA (1.2 x 10(-8) mol) or ISE (4.8 x 10(-5) mol). (5) In conclusion, these findings may indicate the existence of a recognition site specific for taurine, responsible for its effects on thermoregulation.

Animals↗
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↗
PubMed1977

Influence of hepatic taurine concentration on bile acid conjugation with taurine.

In vitro, addition of taurine to liver homogenates increases the proportion of cholic acid conjugated with taurine. In the present study, the relation between hepatic taurine concentration and the proportion of infused sodium cholate conjugated with taurine was studied in the whole organ. The isolated perfused liver was studied to eliminate possible transfer of taurine to or from the large extrahepatic poosl present in vivo. During cholate infusion, the proportion of taurocholate excreted in bile decreased, and the proportion of glycocholate increased in a complementary fashion. Infusion of taurine with cholate prevented these changes. Hepatic taurine concentration, calculated from measured hepatic taurine concentrations before and at the end of cholate infusion, fell. Fall in proportion of total bile acid excreted as taurocholate was most rapid at low hepatic taurine concentrations between about 1.4 and 0.65 mumol/g liver. Hepatic taurine concentrations is a major determinant of the proportion of bile acid conjugated with taurine.

Animals↗
PubMed1988

Colocalization of taurine- and cysteine sulfinic acid decarboxylase-like immunoreactivity in the cerebellum of the rat with monoclonal antibodies against taurine.

Two monoclonal antibodies against fixative-modified taurine, Tau1 and Tau2, were produced, characterized, and used in the present study to analyze the distribution of taurine in the cerebellum of the rat. In addition, immunohistochemical colocalization experiments were performed to determine whether cerebellar neurons contain both taurine and its synthesizing enzyme, cysteine sulfinic acid decarboxylase (CSADC). In ELISAs, both Tau1 and Tau2 displayed high affinities for taurine conjugated to various carrier proteins and possessed some cross-reactivity for other amino acids which are present in lower concentrations in the brain than taurine. Tau2 was found to recognize only taurine and hypotaurine when paraformaldehyde was used to fix the amino acids to carrier proteins. With the use of glutaraldehyde fixation, Tau1 cross-reacted with conjugates of beta-alanine and hypotaurine and Tau2 cross-reacted strongly with conjugates of cysteic acid and hypotaurine and weakly with cysteine sulfinic acid. Despite different cross-reactivities, Tau1 and Tau2 exhibited almost identical patterns of neuronal staining in bands of Purkinje cells in the cerebellum. Staining of Purkinje cell dendrites was more prominent than staining of the soma. Light immunoreactivity was present in Golgi, stellate, and basket cells. A scattered population of granule cells displayed taurine-like immunoreactivity at the electron microscopic level. Immunostaining was identified in some terminals in the Purkinje cell layer and in a limited number of mossy fibers. Tau2-like immunoreactivity was colocalized with CSADC-like immunoreactivity in the cerebellar neurons described above. These immunoreactive cells may represent a subpopulation of neurons that contain a higher concentration of taurine than neighboring cells due to their ability to synthesize taurine. The intense immunoreactive staining of Purkinje cell dendrites provides support for the hypothesis that calcium-dependent release of taurine in the cerebellum may originate primarily from dendritic rather than synaptic processes and suggests a neuromodulator role for taurine in the cerebellum.

Animals↗
PubMed1995

Taurine analog modulation of taurine uptake by two different mechanisms in cultured glial cells.

Previous data have shown that HEPES, a taurine structural analog, inhibits the uptake of taurine by cultured cells differently, depending on its addition either to the culture medium or to the Krebs-Ringer buffer used for cell incubation during taurine uptake measurements (Lleu and Rebel, J Neurosci Res 23: 78-86, 1989). An extensive study of the effect of numerous other taurine structural analogs on taurine uptake by cultured glial cells was carried out. Our results show that taurine uptake modulation by structural analogs follows two different mechanisms. For the first mechanism, observable after the simultaneous presence of taurine and of its analog during the incubation time of the uptake experiment (10 min), the amine function on the molecule is essential. The sulfonate group could be replaced either by a sulfinic group or by a carboxylic group. beta-Alanine, hypotaurine, acetyltaurine, guanidinoethanesulfonate and guanidinopropionate are the most potent inhibitors in this first mechanism. For the second mechanism, which requires the presence of the analog in the culture medium during the 48 hr preceding the taurine uptake measurement, the simultaneous presence of an amine and of a sulfonate group or of an amine and a sulfinate group is required. Carboxylates are ineffective in modulating taurine uptake in this mechanism. The sulfonate buffers synthesized by Good et al. (Biochemistry 5: 467-477, 1966) also affect taurine uptake in both mechanisms.

Animals↗
PubMed2006

Taurine status and response to intravenous taurine supplementation in adults with short-bowel syndrome undergoing long-term parenteral nutrition: a pilot study.

Taurine deficiency in patients on long-term parenteral nutrition may be involved in cholestasis. We aimed to assess plasma taurine and tauro-conjugated bile acids in adults with short-bowel syndrome and their response to intravenous taurine. Thirty-two adult patients, who had been on taurine-free parenteral nutrition for a mean of 59 (SE 14) months for short-bowel syndrome, were studied retrospectively. In a second study, a subgroup of ten patients with chronic cholestasis received taurine-enriched (6.0 (SE 0.6) mg/kg per d) parenteral nutrition for 55 (SE 13) months. Post-absorptive plasma taurine and bile acid concentrations were measured and liver function tests routinely sampled. At baseline, plasma taurine was lower in patients with a jejunal length of less than 35 cm (group A, n 16) than in those with a jejunal length of 35 cm or more (group B, n 16): 43 (SE 3) v. 58 (SE 4) micromol/l (P=0.01). The groups were no different in terms of chronic cholestasis (12/16 v.13/16 patients), total bile acids (26 (SE 13) v.14 (SE 5) micromol/l) or the ratio of tauro-conjugated:glyco-conjugated bile acids (5 (SE 2) v.8(SE 4)%, usual range 30-60%). After supplementation, there was an increase in plasma taurine level (63 (SE 8) v. 43 (SE 4), P=0.007) but was no change in either total bile acids or the ratio of tauro-conjugated: glyco-conjugated bile acids. There was a significant decrease in aspartate aminotransferase level. Long-term parenteral nutrition for short-bowel syndrome is associated with an impaired tauro-conjugation of bile acids (enterohepatic pool), irrespective of plasma taurine level (systemic pool) and despite long-term taurine intravenous supplementation.

Adult↗
PubMed2006

Low plasma taurine concentration in Newfoundland dogs is associated with low plasma methionine and cyst(e)ine concentrations and low taurine synthesis.

Although taurine is not dietarily essential for dogs, taurine deficiency and dilated cardiomyopathy (DCM) are sporadically reported in large-breed dogs. Taurine status and husbandry were examined in 216 privately owned Newfoundlands, a giant dog breed with high incidence of idiopathic DCM (1.3-2.5%). Plasma taurine concentration was positively correlated (P < 0.01) with plasma cyst(e)ine (r = 0.37) and methionine (r = 0.35) concentrations and was similar across age, sex, neutering status, body weight, and body-condition scores. Plasma taurine concentration was low (< or =40 micromol/L) in 8% of dogs. Dogs with low plasma taurine were older, less active, had more medical problems and treatments, and had lower plasma albumin, cyst(e)ine, tryptophan, and alpha-amino-n-butyric acid concentrations than the other dogs (P < 0.05). Of 9 taurine-deficient, clinically evaluated dogs, 3 had DCM that was reversed by taurine supplementation and 1 had retinal degeneration. When given a diet apparently adequate in sulfur amino acids (5.4 g/kg) for 3 wk, 6 Newfoundlands (52.5 +/- 2.3 kg, 3.5-7 y), compared with 6 Beagles (13.2 +/- 2.3 kg, 5.5 y), had lower (P < 0.01) concentrations of plasma taurine (49 +/- 16 vs. 97 +/- 25 micromol/L) and cyst(e)ine and blood glutathione, lower (P < 0.01) de novo taurine synthesis (59 +/- 15 vs. 124 +/- 27 mg x kg(-0.75) x d(-1)), and greater (P < 0.05) fecal bile acid excretion (1.7 +/- 0.2 vs. 1.4 +/- 0.2 micromol/g). Newfoundlands would appear to have a higher dietary sulfur amino acid requirement than Beagles, a model breed used in nutrient requirement determinations.

Animals↗
PubMedDate not supplied

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.

Bile Acids and Salts↗
PubMedDate not supplied

Results of the multicenter spaniel trial (MUST): taurine- and carnitine-responsive dilated cardiomyopathy in American cocker spaniels with decreased plasma taurine concentration.

Fourteen American Cocker Spaniels (ACS) with dilated cardiomyopathy (DCM) were studied to determine if individuals of this breed with DCM are systemically taurine- or carnitine-deficient and to determine if they are responsive to taurine and carnitine supplementation. American Cocker Spaniels with DCM were identified using echocardiography, and plasma was analyzed for taurine and carnitine concentrations. Each dog was randomly assigned to receive either taurine and carnitine supplementation or placebos. Echocardiograms and clinical examinations were repeated monthly for 4 months. During this period, the investigators and owners were blinded with respect to the treatment being administered. Each dog was weaned off its cardiovascular drugs (furosemide, digoxin, and an angiotensin converting enzyme inhibitor) if an echocardiographic response was identified. At the 4-month time period, each investigator was asked to decide whether he or she thought his or her patient was receiving placebo or taurine/carnitine, based on presence or absence of clinical and echocardiographic improvement. Unblinding then occurred, and dogs receiving placebos were switched to taurine and carnitine supplementation and followed monthly for 4 additional months. All dogs were reexamined 6 months after starting supplementation; survival time and cause of death were recorded for each dog. Data from 3 dogs were not included because of multiple protocol violations. Each dog had a plasma taurine concentration < 50 nmol/mL (mean +/- SD for the group 15 +/- 17 nmol/ mL) at baseline; normal range, 50-180 nmol/mL. The plasma taurine concentration did not exceed 50 nmol/mL at any time in the dogs receiving placebos (n = 5), but increased to 357 +/- 157 nmol/mL (range 140-621 nmol/mL) during taurine and carnitine supplementation (n = 11). Plasma carnitine concentration was within, only slightly below, or slightly above reported limits of normality at baseline (29 +/- 15 mumol/L); did not change during placebo administration; and increased significantly during supplementation (349 +/- 119 mumol/L; n = 11). Echocardiographic variables did not change during placebo administration. During supplementation, left ventricular end-diastolic and end-systolic diameters, and mitral valve E point-to-septal separation decreased significantly in both groups. Shortening fraction increased significantly but not into the normal range. Echocardiographic variables remained improved at 6 months. All dogs were successfully weaned off furosemide, an angiotensin converting enzyme inhibitor, and digoxin once an echocardiographic response was identified. Nine of the dogs have died since the onset of the study in 1992. One dog died of recurrence of DCM and heart failure 31 months after starting supplementation; six dogs died of noncardiac causes. Two dogs developed degenerative mitral valve disease and died of complications of this disease. Dogs less than 10 years of age lived for 46 +/- 11 months, whereas dogs older than 10 years of age lived for 14 +/- 7 months. Two of the 11 dogs were alive at the time of publication, having survived for 3.5 and 4.5 years, respectively. We conclude that ACS with DCM are taurine-deficient and are responsive to taurine and carnitine supplementation. Whereas myocardial function did not return to normal in most dogs, it did improve enough to allow discontinuation of cardiovascular drug therapy and to maintain a normal quality of life for months to years.

Administration, Oral↗
PubMed1992

Taurine and osmoregulation. IV. Cerebral taurine transport is increased in rats with hypernatremic dehydration.

Taurine is an organic osmolyte in brain cells. We studied whether cerebral taurine transport is enhanced as part of the cell volume regulatory adaptation to hypernatremia. Hypernatremic dehydration was induced for 48 h. Synaptosomes, metabolically active nerve terminal vesicles, were isolated by homogenization of brain and purification on a discontinuous Ficoll gradient. Taurine transport was evaluated in vitro using a rapid filtration assay. After 48 h of hypernatremia, there was a 22.4% increment in Na(+)-specific taurine transport from 2.99 +/- 0.16 to 3.66 +/- 0.13 mumol/mg protein/30 min (p less than 0.001). Dehydration for 48 h without hypertonic saline loading had no effect on taurine uptake. Glycine transport was unaltered by hypernatremia. The adaptation in taurine uptake resulted from an enhanced Vmax of the high affinity-low capacity transport system [265 +/- 17, control versus 337 +/- 19 nmol/min/mg protein, experimental (p less than 0.03)] without a change in the Km (approximately 60 microM). Under both control and hypernatremic conditions, Na+ and Cl- were required for maximal total Na(+)-mediated taurine uptake. Oubain (1 mM) decreased taurine uptake by 25%, whereas addition of beta-alanine or hypotaurine (500 microM) to the external media reduced taurine transport by 45-65% in both control and experimental conditions (p less than 0.01). Synaptosomal taurine uptake in hypernatremic rats was inhibited by 15-20% (p less than 0.01) after addition of 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) to the external medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Taurine in the liver. The function of taurine conjugated with bile acids.

1. Taurine had cytoprotective effects on hepatocytes under hyperoxic or hypoxic condition in the presence of Ca2+. 2. Bile acids had toxic effects on hepatocytes; there was no significant difference in the toxicity between free bile acids and taurine-conjugated bile acids. 3. The mobility of the membranes, examined by 31P-NMR, decreased after treatment with taurine or free bile acids, but increased after treatment with taurine-conjugated bile acids. 4. The fluidity of the membranes, measured by ESR, did not change after treatment with taurine, but decreased after treatment with free bile acids and increased after treatment with taurine-conjugated bile acids. In conclusion, because most bile acids are conjugated with taurine in the liver after administration of taurine, the influence of taurine-conjugated bile acids has to be taken into consideration in estimating the functions of taurine in the liver.

Animals↗