Taurine Abstracts 10

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Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial.
            (Azuma et al., 1985) Download
In a double-blind, randomized, crossover, placebo-controlled study, we investigated the effects of adding taurine to the conventional treatment in 14 patients with congestive heart failure for a 4-week period. Compared with placebo, taurine significantly improved the New York Heart Association functional class (p less than 0.02), pulmonary crackles (p less than 0.02), and chest film abnormalities (p less than 0.01). A benefit of taurine over placebo was demonstrated when an overall treatment response for each patient was evaluated on the basis of clinical examination (p less than 0.05). No patient worsened during taurine administration, but four patients did during placebo. Pre-ejection period (corrected for heart rate) decreased from 148 +/- 14 ms before taurine treatment to 137 +/- 12 ms after taurine (p less than 0.001), and the quotient pre-ejection period/left ventricular ejection time decreased from 47 +/- 9 to 42 +/- 8% (p less than 0.001). Side effects did not occur in the patients during taurine. The results indicate that addition of taurine to conventional therapy is safe and effective for the treatment of patients with congestive heart failure.

Pancreatic disease: a casualty of hepatic "detoxification"
            (Braganza, 1983) Download
The rising incidence of pancreatic disease suggests that environmental factors are involved: the susceptibility of only a small proportion of individuals indicates that host factors are important. It is postulated that aberrant function of the hepatic mixed-function oxidases (MFOs) is the root cause of pancreatic disease. The MFO system processes numerous chemicals and is induced by many of them: suspected aetiological factors in pancreatic disease (drugs, cigarettes, alcohol, coffee) are inducers of the system. The degree of inducibility is governed by an individual's genetic endowment, and induction is facilitated by an ample supply of dietary polyunsaturated fatty acids. An increase in dietary polyunsaturated fat might explain the rising incidence of pancreatic disease. It is suggested that the products of hepatic "detoxification" (lipid peroxidation products, toxic epoxides, carcinogens, free radicals) are excreted in bile, reflux into the pancreatic duct, and induce pathological changes. Factors that promote reflux would increase risk of disease only when bile contains excessive amounts or abnormal types of reactive intermediates.

Antidepressant dose of taurine increases mRNA expression of GABAA receptor α2 subunit and BDNF in the hippocampus of diabetic rats.
            (Caletti et al., 2015) Download
Diabetes mellitus is a metabolic disorder associated with higher risk for depression. Diabetic rats present depressive-like behaviors and taurine, one of the most abundant free amino acids in the brain, reverses this depressive behaviors. Because taurine is a GABAA agonist modulator, we hypothesize that its antidepressant effect results from the interaction on this system by changing α2 GABAA receptor subunit expression, beside changes on BDNF mRNA, and memory in diabetic rats. Streptozotocin-diabetic and non-diabetic Wistar rats were daily injected with 100mg/kg of taurine or saline, intraperitoneally, for 30 days. At the end of the experiment, rats were exposed to the novel object recognition memory. Later they were euthanized, the brains were weighed, and the hippocampus was dissected for α2 GABAA subunit and BDNF mRNA expression. Real-time quantitative PCR (qPCR) showed that diabetic rats presented lower α2 GABAA subunit and BDNF mRNA expression than non-diabetic rats and taurine increased both parameters in these sick rats. Taurine also reversed the lower brain weight and improved the short-term memory in diabetic rats. Thus, the taurine antidepressant effect may be explained by interference with the GABA system, in line to its neuroprotective effect showed here by preventing brain weight loss and improving memory in diabetic rats.

Functional implication of taurine in aging.
            (El Idrissi et al., 2009b) Download
Age-related impairment of central functions is though to result from alterations of neurochemical indices of synaptic function. These neurochemical modifications involve structural proteins, neurotransmitters, neuropeptides and related receptors. Several studies demonstrated that GABA receptors, glutamic acid decarboxylase (GAD65&67), and different subpopulations of GABAergic neurons are markedly decreased in experimental animal brains during aging. Thus, the age-related decline in cognitive functions could be attributable, at least in part, to decrements in the function of the GABAergic inhibitory neurotransmitter system. In this study we show that chronic supplementation of taurine to aged mice significantly ameliorated the age-dependent decline in memory acquisition and retention, and caused alterations in the GABAergic system. These changes include increased levels of the neurotransmitters GABA and glutamate, increased expression of glutamic acid decarboxylase and the neuropeptide somatostatin and increased in the number of somatostatin-positive neurons. These specific alterations of the inhibitory system caused by taurine treatment oppose those naturally-occurring during aging, and suggest a protective role of taurine in this process. Increased understanding of age-related neurochemical changes in the GABAergic system will be important in elucidating the underpinnings of the functional changes of aging. Taurine might help forestall the age-related decline in cognitive functions through interaction with the GABAergic system.

Taurine supplementation and pancreatic remodeling.
            (El Idrissi et al., 2009a) Download
Taurine is a semi-essential sulphur containing amino acid derived from methionine and cysteine metabolism. Taurine has several biological processes such as hypoglycemic action, antioxidation, and detoxification. In this study we evaluated the role of taurine in pancreatic islets development, since the endocrine pancreas undergoes significant modifications during neonatal life. Histological examination of the pancreas from taurine-fed mice revealed no histological abnormalities in the endocrine or exocrine parts of the pancreas. However, supplementation of taurine in the drinking water resulted in a drastic and significant increase in the number of islets per section. Furthermore, islets size was significantly larger. We hypothesize that supplementation of taurine, which is important for the development of the endocrine pancreas may reduce cytokine-induced apoptosis in pancreatic beta cells. The endocrine pancreas undergoes significant modifications during neonatal life and apoptosis is an important mechanism in this remodeling. We suggest that alteration of this remodeling process during this period of time, when a fine balance between cell replication and cell death is critical, would affect the development of the pancreatic islets of Langerhans, and could have important effects on the pancreatic cell mass and the endocrine function.

Taurine-induced diuresis and natriuresis in cirrhotic patients with ascites.
            (Gentile et al., 1994) Download
Taurine is a non-protein sulfur amino acid widely distributed in mammalian tissues, with poorly understood functions. Taurine administration has a variety of hemodynamic effects, including improvement of cardiac function and suppression of sympathetic activity. Increased urinary volume and sodium excretion have been reported in taurine-fed hamsters. Since patients with ascitic liver cirrhosis have severe hemodynamic and renal abnormalities potentially sensitive to taurine feeding, we evaluated the effects of the i.v. infusion of taurine on urinary flow and sodium excretion and on the hormones involved in the control of hydrosaline homeostasis. Eight cirrhotic patients with tense ascites were given an i.v. bolus of taurine (16 mumoles in 40 ml of saline). The next day patients were given saline only, as a control. Diuresis, urinary sodium and plasma renin activity, aldosterone, atrial natriuretic peptide and arginine vasopressin were measured for the following 6 hrs. Plasma taurine increased ten fold after infusion, then decreased exponentially. No side effects were recorded. After taurine, but not after saline, there was a prompt and significant increase in both urinary volume and sodium excretion. Diuresis increased from 340 +/- 43 to 817 +/- 116 microliters/min (p < 0.01); urinary sodium from 13.8 +/- 3 to 26.3 +/- 4 mumoles/min (p < 0.05). Both values returned to normal after 2-3 hrs. Taurine infusion caused a concomitant significant decrease in plasma renin activity (from 7.7 +/- 2.2 to 4.3 +/- 1.9 ng/ml/hr, p < 0.05) and aldosterone (from 588 +/- 47 to 348 +/- 89 pg/ml, p < 0.05), but no changes in atrial natriuretic peptide and arginine vasopressin. We conclude that i.v. taurine infusion in ascitic cirrhosis promotes a transient diuresis and natriuresis, apparently through the inhibition of the renin-aldosterone axis.

The quest for an animal model of diabetic nephropathy and the role of taurine deficiency.
            (Han et al., 2015) Download
To summarize, the TauT null mouse can serve as an excellent platform on which to create a STZ-induced animal model of diabetic nephropathy. This model mimics numerous features of human diabetic nephropathy, including its clinical aspects and prototypic renal histologic findings. Results from this study also strongly suggest that the malfunction of the taurine transporter found in diabetes patients is an important risk factor for developing kidney disease, including diabetic nephropathy. Thus, one can use this model to design relevant studies and gain greater insight into the causes and consequences of human diabetic nephropathy.

Taurine supplementation prevents the adverse effect of high sugar intake on arterial pressure control after cardiac ischemia/reperfusion in female rats.
            (Kulthinee et al., 2015) Download
High sugar intake affects arterial pressure control mechanisms and taurine supplementation can prevent or improve this adverse effect of high sugar intake. Although high sugar intake starting from weaning onwards may not affect autonomic and baroreflex functions in adult male and female rats, it can impair these functions in rats receiving cardiac IR. High sugar intake depresses baroreflex sensitivity and increases cardiac injury after cardiac IR induction without any effect on autonomic activity in males, while in females, it depresses baroreflex sensitivity, increases sympathetic and decreases parasympathetic activity without any effect on cardiac injury. Further, the present study indicates that short-term taurine supplementation prevents cardiac injury independent of high sugar intake and abolishes the adverse effect of high sugar intake on autonomic and baroreflex function, and on heart rate. These data support the hypothesis that taurine supplementation possesses a benefi- cial action on cardiac function and cardiovascular control after cardiac IR.


 

Taurine regulates insulin release from pancreatic beta cell lines.
            (L'Amoreaux et al., 2010) Download
BACKGROUND:  Pancreatic beta-cells release insulin via an electrogenic response triggered by an increase in plasma glucose concentrations. The critical plasma glucose concentration has been determined to be approximately 3 mM, at which time both insulin and GABA are released from pancreatic beta-cells. Taurine, a beta-sulfonic acid, may be transported into cells to balance osmotic pressure. The taurine transporter (TauT) has been described in pancreatic tissue, but the function of taurine in insulin release has not been established. Uptake of taurine by pancreatic beta-cells may alter membrane potential and have an effect on ion currents. If taurine uptake does alter beta-cell current, it might have an effect on exocytosis of cytoplasmic vesicle. We wished to test the effect of taurine on regulating release of insulin from the pancreatic beta-cell. METHODS:  Pancreatic beta-cell lines Hit-TI5 (Syrian hamster) and Rin-m (rat insulinoma) were used in these studies. Cells were grown to an 80% confluence on uncoated cover glass in RPMI media containing 10% fetal horse serum. The cells were then adapted to a serum-free, glucose free environment for 24 hours. At that time, the cells were treated with either 1 mM glucose, 1 mM taurine, 1 mM glucose + 1 mM taurine, 3 mM glucose, or 3 mM glucose + 1 mM taurine. The cells were examined by confocal microscopy for cytoplasmic levels of insulin. RESULTS:  In both cell lines, 1 mM glucose had no effect on insulin levels and served as a control. Cells starved of glucose had a significant reduction (p<0.001) in the level of insulin, but this level was significantly higher than all other treatments. As expected, the 3 mM glucose treatment resulted in a statistically lower (p<0.001) insulin level than control cells. Interestingly, 1 mM taurine also resulted in a statistically lower level of insulin (p<0.001) compared to controls when either no glucose or 1 mM glucose was present. Cells treated with 1 mM taurine plus 3 mM glucose showed a level of insulin similar to that of 3 mM glucose alone. CONCLUSIONS:  Taurine administration can alter the electrogenic response in beta-cell lines, leading to a change in calcium homeostasis and a subsequent decrease in intracellular insulin levels. The consequence of these actions could represent a method of increasing plasma insulin levels leading to a decrease in plasma glucose levels.

Taurine enhances proliferation and promotes neuronal specification of murine and human neural stem/progenitor cells.
            (Pasantes-Morales et al., 2015) Download
Results from our studies here revised show that restoration of taurine levels in cultured NPCs up to the level found in fresh tissue, has a beneficial effect increasing the number of cells in cultures. A variety of experimental approaches, including gene expression analysis, led us to conclude that taurine is positively influencing the mitochondrial performance, improving the ability of cells to transit into the phases of proliferation cycle. Taurine also increased the number of neurons formed after differentiation of NPCs. This effect may also be a consequence of a more efficient mitochondrial operation, thus increasing neuronal viability, which is known to be highly dependent on a good energy supply

Hereditary mental depression and Parkinsonism with taurine deficiency.
            (Perry et al., 1975) Download
An unusual neuropsychiatric disorder inherited in autosomal dominant fashion occurred in three successive generations of a family. Symptoms commenced late in the fifth decade in six affected patients and led to death in four to six years. The earliest and most prominent symptom was mental depression not responsive to antidepressant drugs or electroconvulsive therapy. This was accompanied by exhaustion, sleep disturbances, and marked weight loss. Later in the disease, symptoms of parkinsonism appeared, and respiratory failure occured terminally. The most recently affected family member was investigated biochemically late in his illness. Concentrations of taurine were greatly diminished in plasma and cerebrospinal fluid, and at autopsy, all regions of brain examined had a markedly reduced taurine content. Since taurine is a putative inhibitory synaptic transmitter, deficiency of brain taurine may possibly have caused the psychiatric and neurological manifestations of this disorder.

Oxidative stress and inflammation in obesity after taurine supplementation: a double-blind, placebo-controlled study.
            (Rosa et al., 2014) Download
PURPOSE:  Some researchers found decreased levels of plasma taurine in obese subjects and animals, and reduced expression of an important enzyme of taurine synthesis. These evidences, coupled with the metabolic imbalance of obesity and the possible anti-inflammatory and antioxidant effects of taurine, highlighted the use of taurine as a supplement in obesity treatment. The aim of the present study was to investigate whether taurine supplementation, associated with nutritional counseling, modulates oxidative stress, inflammatory response, and glucose homeostasis in obese women. METHODS:  A randomized double-blind placebo-controlled study was conducted with 16 women with obesity diagnosis and 8 women in the normal weight range. The obese volunteers were matched by age and body mass index and randomly assigned to either the placebo (3 g/day starch flour) or taurine (3 g/day taurine) group. The study lasted 8 weeks, and the experimental protocol included nutritional assessment and determination of plasma sulfur amino acids, insulin, and adiponectin, serum glycemia, and markers of inflammatory response and oxidative stress. RESULTS:  Plasma taurine levels were significantly decreased (41%) in the obese volunteers. Both the placebo and taurine groups showed significant reduction in weight (3%), with no differences between groups. Different from placebo, taurine-supplemented group showed significant increase in plasma taurine (97%) and adiponectin (12%) and significant reduction in the inflammatory marker hs-C-reactive protein (29%) and in the lipid peroxidation marker thiobarbituric acid reactive substances (TBARS) (20%). CONCLUSIONS:  Eight weeks of taurine supplementation associated with nutritional counseling is able to increase adiponectin levels and to decrease markers of inflammation (high-sensitivity C-reactive protein) and lipid peroxidation (TBARS) in obese women.

Taurine in 24-h Urine Samples Is Inversely Related to Cardiovascular Risks of Middle Aged Subjects in 50 Populations of the World.
            (Sagara et al., 2015) Download
We previously showed that 24-h urinary taurine (Tau) excretion was inversely associated with mortality due to coronary heart diseases (CHD) and stroke. The aim of this study was to examine the association between 24-h urinary Tau/creatinine (Cre) ratio and cardiovascular disease risk factors, including body mass index (BMI), blood pressure (BP), serum total cholesterol (TC) and prevalence of obesity, hypertension and hypercholesterolemia.
A cross sectional analysis was conducted among 4,211 participants (2,120 men and 2,091 women) aged 48–56 from 50 population samples of 22 countries in the World Health Organization-coordinated Cardiovascular Diseases and Alimentary Comparison (CARDIAC) Study (1985–1994).
According to linear regression analyses adjusted for traditional risk factors such as age, sex and anti-hypertensive treatment, Tau/Cre was inversely associated with BMI, systolic BP, diastolic BP and TC (P for linear trend <0.001, respectively). These associations were not markedly altered by further adjustment for 24-h urinary sodium/Cre, potassium/Cre, calcium/Cre, magnesium/Cre and cohort effects. After adjusting for the traditional risk factors, the prevalence of obesity, hypertension and hypercholesterolemia among the subjects within the lowest quintile of the Tau/Cre ratio was 2.84 (95 % CI: 2.04, 3.96; P for trend <0.001), 1.22 (95 % CI: 0.98, 1.51; P < 0.05) and 2.20 (95 % CI: 1.73, 2.80; P < 0.001) times higher than that in the subjects within the highest quintile. These associations were not appreciably altered by further adjustment for other 24-h urinary markers and cohort effects.
In conclusion, higher Tau/Cre was associated with lower cardiovascular disease risk factors, including BMI, BP, TC, obesity, hypertension and hypercholesterolemia.

Taurine supplementation ameliorates glucose homeostasis, prevents insulin and glucagon hypersecretion, and controls β, α, and δ-cell masses in genetic obese mice.
            (Santos-Silva et al., 2015) Download
Taurine (Tau) regulates β-cell function and glucose homeostasis under normal and diabetic conditions. Here, we assessed the effects of Tau supplementation upon glucose homeostasis and the morphophysiology of endocrine pancreas, in leptin-deficient obese (ob) mice. From weaning until 90-day-old, C57Bl/6 and ob mice received, or not, 5% Tau in drinking water (C, CT, ob and obT). Obese mice were hyperglycemic, glucose intolerant, insulin resistant, and exhibited higher hepatic glucose output. Tau supplementation did not prevent obesity, but ameliorated glucose homeostasis in obT. Islets from ob mice presented a higher glucose-induced intracellular Ca(2+) influx, NAD(P)H production and insulin release. Furthermore, α-cells from ob islets displayed a higher oscillatory Ca(2+) profile at low glucose concentrations, in association with glucagon hypersecretion. In Tau-supplemented ob mice, insulin and glucagon secretion was attenuated, while Ca(2+) influx tended to be normalized in β-cells and Ca(2+) oscillations were increased in α-cells. Tau normalized the inhibitory action of somatostatin (SST) upon insulin release in the obT group. In these islets, expression of the glucagon, GLUT-2 and TRPM5 genes was also restored. Tau also enhanced MafA, Ngn3 and NeuroD mRNA levels in obT islets. Morphometric analysis demonstrated that the hypertrophy of ob islets tends to be normalized by Tau with reductions in islet and β-cell masses, but enhanced δ-cell mass in obT. Our results indicate that Tau improves glucose homeostasis, regulating β-, α-, and δ-cell morphophysiology in ob mice, indicating that Tau may be a potential therapeutic tool for the preservation of endocrine pancreatic function in obesity and diabetes.

Taurine: new implications for an old amino acid.
            (Schuller-Levis and Park, 2003) Download
Taurine is a semi-essential amino acid and is not incorporated into proteins. In mammalian tissues, taurine is ubiquitous and is the most abundant free amino acid in the heart, retina, skeletal muscle, brain, and leukocytes. In fact, taurine reaches up to 50 mM concentration in leukocytes. Taurine has been shown to be tissue-protective in many models of oxidant-induced injury. One possibility is that taurine reacts with hypochlorous acid, produced by the myeloperoxidase pathway, to produce the more stable but less toxic taurine chloramine (Tau-Cl). However, data from several laboratories demonstrate that Tau-Cl is a powerful regulator of inflammation. Specifically, Tau-Cl has been shown to down-regulate the production of pro-inflammatory mediators in both rodent and human leukocytes. Taurolidine, a derivative of taurine, is commonly used in Europe as an adjunctive therapy for various infections as well as for tumor therapy. Recent molecular studies on the function of taurine provide evidence that taurine is a constituent of biologic macromolecules. Specifically, two novel taurine-containing modified uridines have been found in both human and bovine mitochondria. Studies investigating the mechanism of action of Tau-Cl have shown that it inhibits the activation of NF-kappaB, a potent signal transducer for inflammatory cytokines, by oxidation of IkappaB-alpha at Met45. Key enzymes for taurine biosynthesis have recently been cloned. Cysteine sulfinic acid decarboxylase, a rate-limiting enzyme for taurine biosynthesis, has been cloned and sequenced in the mouse, rat and human. Another key enzyme for cysteine metabolism, cysteine dioxygenase (CDO), has also been cloned from rat liver. CDO has a critical role in determining the flux of cysteine between cysteine catabolism/taurine synthesis and glutathione synthesis. Taurine transporter knockout mice show reduced taurine, reduced fertility, and loss of vision due to severe apoptotic retinal degeneration. Apoptosis induced by amino chloramines is a current and important finding since oxidants derived from leukocytes play a key role in killing pathogens. The fundamental importance of taurine in adaptive and acquired immunity will be unveiled using genetic manipulation.

The neuroprotective effects of taurine against nickel by reducing oxidative stress and maintaining mitochondrial function in cortical neurons.
            (Xu et al., 2015) Download
Previous studies have indicated that oxidative stress and mitochondrial dysfunction are involved in the toxicity of nickel. Taurine is recognized as an efficient antioxidant and is essential for mitochondrial function. To investigate whether taurine could protect against the neurotoxicity of nickel, we exposed primary cultured cortical neurons to various concentrations of nickel chloride (NiCl2; 0.5mM, 1mM and 2mM) for 24h or to 1mM NiCl2 for various periods (0 h, 12h, 24h and 48 h). Our results showed that taurine efficiently reduced lactate dehydrogenase (LDH) release induced by NiCl2. Along with this protective effect, taurine pretreatment not only significantly reversed the increase of ROS production and mitochondrial superoxide concentration, but also attenuated the decrease of superoxide dismutase (SOD) activity and glutathione (GSH) concentration in neurons exposed to NiCl2 for 24h. Moreover, nickel exposure reduced ATP production, disrupted the mitochondrial membrane potential and decreased mtDNA content. These types of oxidative damage in the mitochondria were efficiently ameliorated by taurine pretreatment. Taken together, our results indicate that the neuroprotective effects of taurine against the toxicity of nickel might largely depend on its roles in reducing oxidative stress and improving mitochondrial function. Taurine may have great pharmacological potential in treating the adverse effects of nickel in the nervous system.

High dietary taurine reduces apoptosis and atherosclerosis in the left main coronary artery: association with reduced CCAAT/enhancer binding protein homologous protein and total plasma homocysteine but not lipidemia.
            (Zulli et al., 2009) Download
We sought to determine whether taurine could specifically protect against coronary artery disease during an atherogenic diet and whether taurine affects the lipid profile, metabolites of methionine, and endothelial atherogenic systems. Rabbits were fed one of the following diets for 4 weeks: (1) control diet; (2) 0.5% cholesterol+1.0% methionine; or (3) 0.5% cholesterol+1.0% methionine+2.5% taurine. Endothelial function was examined, and the left main coronary artery atherosclerosis was quantified by stereology and semiquantitative immunohistochemistry to determine the endothelial expression of proteins related to the NO, renin-angiotensin, endoplasmic reticulum, and oxidative stress systems, as well as apoptosis. Taurine normalized hyperhomocysteinemia (P<0.05) and significantly reduced hypermethioninemia (P<0.05) but not lipidemia. The intima:media ratio was reduced by 28% (P=0.034), and atherosclerosis was reduced by 64% (P=0.012) and endothelial cell apoptosis by 30% (P<0.01). Endothelial cell CCAAT/enhancer binding protein homologous protein was normalized (P<0.05). Taurine failed to improve hyperlipidemia, endothelial function, or endothelial proteins related to the NO, renin-angiotensin, and oxidative stress systems. Taurine reduces left main coronary artery wall pathology associated with decreased plasma total homocysteine, methionine, apoptosis, and normalization of CCAAT/enhancer binding protein homologous protein. These results elucidate the antiapoptotic and antiatherogenic properties of taurine, possibly via normalization of endoplasmic reticulum stress.

 


References

Azuma, J, et al. (1985), ‘Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial.’, Clin Cardiol, 8 (5), 276-82. PubMed: 3888464
Braganza, JM (1983), ‘Pancreatic disease: a casualty of hepatic “detoxification”’, Lancet, 2 (8357), 1000-3. PubMed: 6138545
Caletti, G, et al. (2015), ‘Antidepressant dose of taurine increases mRNA expression of GABAA receptor α2 subunit and BDNF in the hippocampus of diabetic rats.’, Behav Brain Res, 283 11-15. PubMed: 25612506
El Idrissi, A, L Boukarrou, and W L’Amoreaux (2009a), ‘Taurine supplementation and pancreatic remodeling.’, Adv Exp Med Biol, 643 353-58. PubMed: 19239166
El Idrissi, A, et al. (2009b), ‘Functional implication of taurine in aging.’, Adv Exp Med Biol, 643 199-206. PubMed: 19239150
Gentile, S, et al. (1994), ‘Taurine-induced diuresis and natriuresis in cirrhotic patients with ascites.’, Life Sci, 54 (21), 1585-93. PubMed: 8196477
Han, X, et al. (2015), ‘The quest for an animal model of diabetic nephropathy and the role of taurine deficiency.’, Adv Exp Med Biol, 803 217-26. PubMed: 25833501
Kulthinee, S, JM Wyss, and S Roysommuti (2015), ‘Taurine supplementation prevents the adverse effect of high sugar intake on arterial pressure control after cardiac ischemia/reperfusion in female rats.’, Adv Exp Med Biol, 803 597-611. PubMed: 25833530
L’Amoreaux, WJ, et al. (2010), ‘Taurine regulates insulin release from pancreatic beta cell lines.’, J Biomed Sci, 17 Suppl 1 S11. PubMed: 20804585
Pasantes-Morales, H, G Ramos-Mandujano, and R Hernández-Benítez (2015), ‘Taurine enhances proliferation and promotes neuronal specification of murine and human neural stem/progenitor cells.’, Adv Exp Med Biol, 803 457-72. PubMed: 25833518
Perry, TL, et al. (1975), ‘Hereditary mental depression and Parkinsonism with taurine deficiency.’, Arch Neurol, 32 (2), 108-13. PubMed: 1122173
Rosa, FT, et al. (2014), ‘Oxidative stress and inflammation in obesity after taurine supplementation: a double-blind, placebo-controlled study.’, Eur J Nutr, 53 (3), 823-30. PubMed: 24065043
Sagara, M, et al. (2015), ‘Taurine in 24-h Urine Samples Is Inversely Related to Cardiovascular Risks of Middle Aged Subjects in 50 Populations of the World.’, Adv Exp Med Biol, 803 623-36. PubMed: 25833532
Santos-Silva, JC, et al. (2015), ‘Taurine supplementation ameliorates glucose homeostasis, prevents insulin and glucagon hypersecretion, and controls β, α, and δ-cell masses in genetic obese mice.’, Amino Acids, 47 (8), 1533-48. PubMed: 25940922
Schuller-Levis, GB and E Park (2003), ‘Taurine: new implications for an old amino acid.’, FEMS Microbiol Lett, 226 (2), 195-202. PubMed: 14553911
Xu, S, et al. (2015), ‘The neuroprotective effects of taurine against nickel by reducing oxidative stress and maintaining mitochondrial function in cortical neurons.’, Neurosci Lett, 590 52-57. PubMed: 25637701
Zulli, A, et al. (2009), ‘High dietary taurine reduces apoptosis and atherosclerosis in the left main coronary artery: association with reduced CCAAT/enhancer binding protein homologous protein and total plasma homocysteine but not lipidemia.’, Hypertension, 53 (6), 1017-22. PubMed: 19398656