Mr.kaz
Messages : 3699
Inscription : 19/03/2009
 |  Sujet: Taurine. Lun 24 Mai - 15:22 | |
| Yucca - Citation :
- L'effet excitant cérébral (léger, hein) est à faibles doses (il y en a dans le redbull, 1g je crois) soit 1 à 2g
Au dela de 3g, environ 5 dans mon cas, ça calme: aide à l'endormissement et régulation du rythme cardiaque, comme déjà indiqué. Au delà : j'ai pas trouvé de différence d'effets, donc inutile d'en prendre plus. Mais comme de nombreux acides aminés, l'effet est individuel, donc il faut tester pour se rendre compte... - Citation :
- A propos de la Taurine : j'ai déjà posté pas mal de trucs dans un autre sujet. Il y a énormément d'articles/études en anglais. voir ci dessous pour la liste interminable de ses bienfaits pour un coût dérisoire.
Effets constatés :
-A fortes doses (>3g) sédatif + régulation rapide du rythme cardiaque et effet anti crampes (excellent en récupération d'un exercice physique intensif)
-A faibles doses -environ 1g- excitant cérébral (pas cardiaque)
-Aucun effet secondaire (j'ai testé jusqu'à 10g de poudre sur moi : juste un léger effet sédatif, mais pas supérieur à ce que l'on obtient avec 3 à 5g). C'est un acide aminé que l'on trouve dans la nourriture, pas une molécule pharmaceutique. Les huitres et autres fruits de mer comportent une forte concentration de taurine par ex.
Citation :
Abstract
Taurine is a conditionally-essential amino acid which is not utilized in protein synthesis, but rather is found free or in simple peptides. Taurine has been shown to be essential in certain aspects of mammalian development, and in vitro studies in various species have demonstrated that low levels of taurine are associated with various pathological lesions, including cardiomyopathy, retinal degeneration, and growth retardation, especially if deficiency occurs during development. Metabolic actions of taurine include: bile acid conjugation, detoxification, membrane stabilization, osmoregulation, and modulation of cellular calcium levels. Clinically, taurine has been used with varying degrees of success in the treatment of a wide variety of conditions, including: cardiovascular diseases, hypercholesterolemia, epilepsy and other seizure disorders, macular degeneration, Alzheimer's disease, hepatic disorders, alcoholism, and cystic fibrosis. (Alt Med Rev 1998;3(2):128-136)
--------------------------------------------------------------------------------
Introduction
Taurine (2-aminoethanesulfonic acid, see Figure 1) is a conditionally-essential amino acid which is not utilized in protein synthesis, but rather is found free or in simple peptides. First discovered as a component of ox bile in 1827, it was not until 1975 that the significance of taurine in human nutrition was identified, when it was discovered that formula-fed, pre-term infants were not able to sustain normal plasma or urinary taurine levels.1 Signs of taurine deficiency have also been detected in children on long-term, total parenteral nutrition,2 and in patients with "blind-loop" syndrome.3 In vivo studies in various species have shown taurine to be essential in certain aspects of mammalian development, and have demonstrated that low levels of taurine are associated with various pathological lesions, including cardiomyopathy, retinal degeneration, and growth retardation, especially if deficiency occurs during development.4
Derived from methionine and cysteine metabolism, taurine is known to play an important role in numerous physiological functions. While conjugation of bile acids is perhaps its best-known function, this accounts for only a small proportion of the total body pool of taurine in humans. Other metabolic actions of taurine include: detoxification, membrane stabilization, osmoregulation, and modulation of cellular calcium levels. Clinically, taurine has been used in the treatment of a wide variety of conditions, including: cardiovascular diseases, epilepsy and other seizure disorders, macular degeneration, Alzheimer's disease, hepatic disorders, and cystic fibrosis. An analog of taurine, acamprosate, has been used as a treatment for alcoholism.
--------------------------------------------------------------------------------
.....
--------------------------------------------------------------------------------
Cardiovascular Effects
Taurine comprises over 50 percent of the total free amino acid pool of the heart.9 It has a positive inotropic action on cardiac tissue,10 and has been shown in some studies to lower blood pressure.11,12 In part, the cardiac effects of taurine are probably due to its ability to protect the heart from the adverse effects of either excessive or inadequate calcium ion (Ca2+) levels.13 The consequence of Ca2+ excess is the accumulation of intracellular calcium, ultimately leading to cellular death. Taurine may both directly and indirectly help regulate intracellular Ca2+ ion levels by modulating the activity of the voltage-dependent Ca2+ channels, and by regulation of Na+ channels. Taurine also acts on many other ion channels and transporters. Therefore, its action can be quite non-specific.14 When an adequate amount of taurine is present, calcium-induced myocardial damage is significantly reduced, perhaps by interaction between taurine and membrane proteins.15 At least one study has suggested taurine's ability to function as a membrane stabilizer is related to its capacity to prevent suppression of membrane-bound NaK ATPase.16
Other research demonstrates taurine can protect the heart from neutrophil-induced reperfusion injury and oxidative stress. Because the respiratory burst activity of neutrophils is also significantly reduced in the presence of taurine, perhaps taurine's protective effect is mediated by its antioxidative properties.17
Azuma and associates have observed that taurine alleviates physical signs and symptoms of congestive heart failure (CHF).18-20 Chazov et al were able to demonstrate that taurine could reverse EKG abnormalities such as S-T segment changes, T-wave inversions, and extra systoles in animals with chemically-induced arrhythmias.21
A double-blind, placebo-controlled crossover study suggested, "taurine is an effective agent for the treatment of heart failure without any adverse effects." 22 Fourteen patients (9 men and 5 women) with CHF were evaluated initially and baseline data were obtained. Patients were assigned a "heart-failure score" based on the degree of dyspnea, pulmonary sounds, signs of right-heart failure, and chest film abnormalities. All patients were continued on digitalis with diuretics and/or vasodilators throughout the study period. Patients received 6 grams per day in divided doses of either taurine or placebo for four weeks, followed by a 2-week "wash-out" period. Prior to the cross-over period, baseline data were obtained for the following study period, in which patients received placebo or taurine, whichever was not taken during the first study period. Heart-failure scores fell from 5.8 ± 0.7 before taurine administration to 3.7 ± 0.5 after taurine (p < 0.001); the score did not change significantly during the placebo period. A "favorable response was observed in 79 percent (11/14 patients) during the taurine-treated period and in 21 percent (3/14 patients) during the placebo-treated period; 4 patients worsened during the placebo period, whereas none did during the taurine period (p less than 0.05)."22
Research has also been conducted in animals to determine whether oral taurine increased survivability in CHF which resulted from surgically-induced aortic regurgitation. Albino rabbits received either taurine (100 mg/kg) or placebo after surgical damage to the aortic cusps, which produced aortic regurgitation. "Cumulative mortality at 8 weeks of non-treated rabbits following aortic regurgitation was 52% (12/23 animals) compared with 11% (1/9 animals) in taurine-treated group (p less than 0.05)... Taurine prevented the rapid progress of congestive heart failure induced artificially by aortic regurgitation, and consequently prolonged the life expectancy." 23
--------------------------------------------------------------------------------
Bile Acid Conjugation and Cholesterol Excretion
The liver forms a 2-4 gram bile acid pool that has approximately ten enterohepatic cycles per day, with the terminal ileum serving as the main absorption site for the enterohepatic recycling of approximately 80 percent of these acids. Bile acids function as a detergent for emulsification and absorption of lipids and fat-soluble vitamins. Critical to this function of bile are the bile salts which, because of their lipophilic and hydrophilic components, can lower surface tension and form micelles. Two major bile acids are derived from hepatic cholesterol metabolism: cholic acid and chenodeoxycholic acid. From these primary bile acids, intestinal bacteria form the secondary bile acids deoxycholic acid and lithocholic acid, respectively. For these bile acids to be solubilized at physiological pH, it is essential they be conjugated through peptide linkages with either glycine or taurine; these amino acid conjugates are referred to as bile salts.
Taurine conjugation of bile acids has a significant effect on the solubility of cholesterol, increasing its excretion, and administration of taurine has been shown to reduce serum cholesterol levels in human subjects. In a single-blind, placebo-controlled study, 22 healthy male volunteers, aged 18-29 years, were randomly placed in one of two groups and fed a high fat/high cholesterol diet, designed to raise serum cholesterol levels, for three weeks. The experimental group received 6 grams of taurine daily. At the end of the test period, the control group had significantly higher total cholesterol and LDL-cholesterol levels than the group receiving taurine.24
--------------------------------------------------------------------------------
Cystic Fibrosis
Most cystic fibrosis (CF) patients suffer from nutrient malabsorption, where much of the insult is in the ileum. Since the terminal ileum serves as the main absorption site for the enterohepatic recycling of approximately 80 percent of bile acids, they are malabsorbed as well. Taurine supplementation has been shown to decrease the severity of steatorrhea associated with many CF cases.25,26 In one double-blind crossover study, 13 CF children with steatorrhea of at least 13 grams per day were treated with a taurine dose of 30 mg/kg/day. The study continued for two consecutive 4-month durations and involved both placebo and treatment periods. Ninety-two percent of the CF children showed decreased fecal fatty acid and sterol excretion while taking taurine.25 In CF patients with a high degree of steatorrhea, bile acid absorption was increased with taurine supplementation, suggesting a possible role for taurine in treating malabsorption.26
--------------------------------------------------------------------------------
Detoxification
Due to its ability to neutralize hypochlorous acid, a potent oxidizing substance, taurine is able to attenuate DNA damage caused by aromatic amine compounds in vitro.27 Because of taurine's unique structure, containing a sulfonic acid moiety rather than carboxylic acid, it does not form an aldehyde from hypochlorous acid, forming instead a relatively stable chloroamine compound. Hence, taurine is an antioxidant that specifically mediates the chloride ion and hypochlorous acid concentration, and protects the body from potentially toxic effects of aldehyde release.
Taurine has also been reported to protect against carbon tetrachloride-induced toxicity.28-31 In rats exposed to carbon tetrachloride (CCl4), hepatic taurine content decreased significantly 12 and 24 hours after CCl4 administration. However, oral administration of taurine to CCl4-exposed rats was able to protect these animals from hepatic taurine depletion, suggesting that hepatic taurine may play a critical role in the protection of hepatocytes against hepatotoxins such as CCl4.28
Exposure to bacterial endotoxins has been suggested as one factor which can augment the magnitude of individual responses to xenobiotics.32 Circulating endotoxins of intestinal origin have been found to create a positive feedback on endotoxin translocation from the gut, stimulating increases in serum endo-toxin levels. In experimental animals, taurine was found to significantly inhibit intestinal translocation and to protect the animals from endotoxemic injury.33 Therefore, it is possible taurine might be able to modify factors underlying susceptibility to toxic chemicals.
--------------------------------------------------------------------------------
Hepatic Disorders
Two groups of patients with acute hepatitis, all with serum bilirubin levels above 3 mg/dl, were studied in a double-blind, randomized protocol. Subjects in the treatment group received 4 grams of taurine three times daily. Bilirubin, total bile acids, and biliary glycine:taurine ratio all decreased significantly in the taurine group within one week as compared to controls.34
--------------------------------------------------------------------------------
Alcoholism
Twenty-two patients undergoing treatment for alcohol withdrawal were given 1 gram of taurine three times per day orally for seven days. When compared to retrospective controls, significantly fewer of the taurine-treated patients had psychotic episodes (14% vs. 45%, p < 0.05). The number of psychotic cases after admission who had also been psychotic before admission was 1/16 for the taurine group and 11/17 for the controls (p < 0.001).35
Recently, acamprosate, a synthetic taurine analog, has been shown to be clinically useful in the treatment of alcohol dependence.36-41 Currently available only in Europe, acamprosate (calcium acetylhomotaurinate) has a chemical structure similar to that of gamma-aminobutyric acid, and is thought to act via several mechanisms affecting multiple neurotransmitter systems, and by modulation of calcium ion fluxes. About 50 percent of alcoholic patients relapse within three months of treatment. In a pooled analysis of data from 11 randomized, placebo-controlled trials involving a total of 3,338 patients with alcohol dependence, those treated with acamprosate showed higher abstinence rates and durations of abstinence during 6- to 12-month post-treatment follow-up periods, when compared to those receiving placebo.36
In a two-year, randomized, double-blind, placebo-controlled study, 272 patients initially were given short-term detoxification treatment, and then received routine counseling and either acamprosate or placebo for 48 weeks, after which they were followed for another 48 weeks without medication. Subjects who received acamprosate showed a significantly higher continuous abstinence rate at the end of the treatment period compared to those who were assigned to the placebo group (43% vs 21%, p = .005), and they had a significantly longer mean abstinence duration of 224 vs 163 days, or 62 percent vs 45 percent days abstinent (p < .001). However, there was no difference in psychiatric symptoms. At the end of a further 48 weeks without receiving study medication, 39 percent and 17 percent of the acamprosate- and placebo-treated patients, respectively, had remained abstinent (p = .003).37
Two in vitro studies have been published comparing the effects of acamprosate and calcium acetyltaurinate on ionic membrane transfer.40,41 Ethanol has been shown to reduce ionic transfer through alterations in the cationic paracellular pathway, the coupling between two adjacent epithelial cells, the monovalent cation pump, and the antiport system. In both of these studies, the results indicate two closely related compounds have different effects on ionic membrane transfer. Therefore, caution should be used in extrapolating the effects of acamprosate to taurine or other taurine analogs.
--------------------------------------------------------------------------------
Ocular Disorders
The retina contains one of the highest concentrations of taurine in the body. In cats, when the retina has been depleted to about one-half its normal taurine content, changes in the photoreceptor cells begin to appear, and further depletion can result in permanent retinal degeneration.42 In some respects, the retinal degeneration seen in the human disease retinitis pigmentosa (RP) is similar to that observed in taurine-deficient cats. However, studies of plasma and platelet taurine levels in patients with RP have yielded very inconsistent results.43-45 A clinical trial of taurine (1-2 g/day) for one year in patients with RP did not result in any laboratory or clinical evidence of improvement, although some subjective benefits were reported.46
--------------------------------------------------------------------------------
Epilepsy
Although several clinical trials involving taurine supplementation in epileptic patients have been reported, most have major methodological flaws.47 Depending on the criteria used, the degree of success reported in various trials using taurine in the treatment of epilepsy has been between 16 and 90 percent.48-56 In these trials, dosages ranged from 375 to 8,000 mg/day. The precise role of taurine in synaptic transmission is uncertain, and its antiepileptic action, confirmed in several models of experimental epilepsy and in short-term clinical studies, does not seem to possess major clinical relevance since trials with a longer follow-up period have generally produced less satisfactory results. Taurine's limited diffusibility across the blood-brain barrier may be the main factor restricting the antiepileptic effect of this compound.
--------------------------------------------------------------------------------
Alzheimer's Disease
Levels of the neurotransmitter acetylcholine have been described as abnormally low in patients with Alzheimer's disease. These insufficient levels are presumed to be related to the memory loss which characterizes the condition, and treatment of Alzheimer's disease based on this premise has been proposed.57 Taurine administered to experimental animals has been able to increase the level of acetylcholine in the brain,58 and researchers have demonstrated that decreased concentrations of taurine are present in the cerebral spinal fluid of patients with advanced symptoms of Alzheimer's disease when compared to age-matched controls.59 To date, no clinical trials on the use of taurine for the treatment of Alzheimer's disease have been reported in the medical literature.
--------------------------------------------------------------------------------
Diabetes
Both plasma and platelet taurine levels have been found to be depressed in insulin-dependent diabetic patients; however, these levels were raised to normal with oral taurine supplementation. In addition, the amount of arachidonic acid needed to induce platelet aggregation was lower in these patients than in healthy subjects. Taurine supplementation reversed this effect as well, reducing platelet aggregation. In vitro experiments demonstrated that taurine reduced platelet aggregation in diabetic patients in a dose-dependent manner, while having no effect on the aggregation of platelets from healthy subjects.
--------------------------------------------------------------------------------
Conclusion
Although it is readily apparent that taurine is important in conjugating bile acids to form water-soluble bile salts, only a fraction of available taurine is used for this function. Taurine is also involved in a number of other crucially important processes, including calcium ion flux, membrane stabilization, and detoxification. Some areas of investigation into the clinical uses of taurine have revealed significant applications for this amino acid: congestive heart failure, cystic fibrosis, toxic exposure, and hepatic disorders. Other conditions such as epilepsy and diabetes will require further research before a clear rationale for the use of taurine can be developed.
--------------------------------------------------------------------------------
References
1. Raiha N, Rassin D, Heinonen K, Gaull GE. Milk protein quality and quantity: Biochemical and growth effects in low birth weight infants (LBWI). Pediatr Res 1975;9:370.
2. Geggel HS, Ament ME, Heckenlively JR, et al. Nutritional requirement for taurine in patients receiving long-term parenteral nutrition. N Engl J Med 1985;312:142-146.
3. Sheik K, Toskes P, Dawson W. Taurine deficiency and retinal defects associated with small intestinal bacterial overgrowth. Gastroenterology 1981;80:1363.
4. Sturman JA. Taurine in development. Physiol Rev 1993;73:119-147.
5. Huxtable RJ. Physiological actions of taurine. Physiol Rev 1992;72:101-163.
6. Shin HK, Linkswiler HM. Tryptophan and methionine metabolism of adult females as affected by vitamin B6 deficiency. J Nutr 1974;104:1348-1355.
7. Hayes KC. Taurine requirement in primates. Nutr Rev 1985;43:65-70.
8. Worden JA, Stipanuk MH. A comparison by species, age and -- censure -- of cysteinesulfinate decarboxylase activity and taurine concentration in liver and brain of animals. Comp Biochem Physiol 1985;82:233-239.
9. Jacobsen JG, Smith LH. Biochemistry and physiology of taurine and taurine derivatives. Physiol Rev 1968;48:424-511.
10. Huxtable RJ and Sebring LA. Cardiovascular actions of taurine. In: Kuriyama K, Huxtable R, Iwata H (eds.), Sulfur Amino Acids: Biochemical and Clinical Aspects. New York:Alan R. Liss;1983:5-37.
11. Nara Y, Yamori Y, Lovenberg W. Effects of dietary taurine on blood pressures in spontaneously hypertensive rats. Biochem Pharmacol 1978;27:2689-2692.
12. Bousquet P, Feldman J, Bloch R, Schwartz J. Central cardiovascular effects of taurine: comparison with homotaurine and muscimol. J Pharmacol Exp Ther 1981;219:213-218.
13. Satoh H. Cardioprotective actions of taurine against intracellular and extracellular Ca2+-induced effects. Adv Exp Med Biol 1994;359:181-196.
14. Satoh H, Sperelakis N. Review of some actions of taurine on ion channels of cardiac muscle cells and others. Gen Pharmac 1998;30:451-463.
15. Kramer JH, Chovan JP, Schaffer SW. Effect of taurine in calcium paradox and ischemic heart failure. Am J Physiol 1981;240:H238-H246.
16. Qi B, Yamagami T, Naruse Y, et al. Effects of taurine on depletion of erythrocyte membrane Na-K ATPase activity due to ozone exposure or cholesterol enrichment. J Nutr Sci Vitaminol 1995;41:627-634.
17. Raschke P, Massoudy P, Becker BF. Taurine protects the heart from neutrophil-induced reperfusion injury. Free Radic Biol Med 1995;19:461-471.
18. Azuma J, Hasegawa H, Sawamura A, et al. Therapy of congestive heart failure with orally administered taurine. Clin Ther 1983;5:398-408.
19. Azuma J, Sawamura A, Awata N, et al. Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial. Clin Cardiol 1985;8:276-282.
20. Azuma J, Sawamura A, Awata K. Usefulness of taurine in chronic congestive heart failure and its prospective application. Jpn Circ J 1992;56:95-99.
21. Chazov EI, Malchikova LS, Lipina NV, et al. Taurine and electrical activity of the heart. Circ Res 1974;35 (Suppl 3):11-21.
22. Azuma J, Takihara K, Awata N, et al. Taurine and failing heart: experimental and clinical aspects. Prog Clin Biol Res 1985;179:195-213.
23. Azuma J, Takihara K, Awata N, et al. Beneficial effect of taurine on congestive heart failure induced by chronic aortic regurgitation in rabbits. Res Commun Chem Path Pharm 1984;45:261-270.
24. Mizushima S, Nara Y, Sawamura M, Yamori Y. Effects of oral taurine supplementation on lipids and sympathetic nerve tone. Adv Exp Med Biol 1996;403:615-622.
25. Smith U, Lacaille F, Lepage G, et al. Taurine decreases fecal fatty acid and sterol excretion in cystic fibrosis. A randomized double-blind study. Am J Dis Child 1991;145:1401-1404.
26. Carrasco S, Codoceo R, Prieto G, et al. Effect of taurine supplements on growth, fat absorption and bile acid on cystic fibrosis. Acta Univ Carol 1990;36:152-156.
27. Kozumbo WJ, Agarwal S, Koren HS. Breakage and binding of DNA by reaction products of hypochlorous acid with aniline, l-naphthylamine or l-naphthol. Toxicol Appl Pharmacol 1992;115:107-115.
28. Nakashima T, Taniko T, Kuriyama K. Therapeutic effect of taurine administration on carbon tetrachloride-induced hepatic injury. Jpn J Pharmacol 1982;32:583-589.
29. Waterfield CJ, Turton JA, Scales MD, Timbrell JA. Reduction of liver taurine in rats by beta-alanine treatment increases carbon tetrachloride toxicity. Toxicology 1993;77:7-20.
30. Timbrell JA, Waterfield CJ. Changes in taurine as an indicator of hepatic dysfunction and biochemical perturbations. Studies in vivo and in vitro. Adv Exp Med Biol 1996;403:125-134.
31. Wu C, Miyagawa C, Kennedy DO, et al. Involvement of polyamines in the protection of taurine against the cytotoxicity of hydrazine or carbon tetrachloride in isolated rat hepatocytes. Chem Biol Interact 1997;103:213-224.
32. Roth RA, Harkema JR, Pestka JP, Ganey PE. Is exposure to bacterial endotoxin a determinant of susceptibility to intoxication from xenobiotic agents? Toxicol Appl Pharmacol 1997;147:300-311.
33. Wang WY. Intestinal endotoxin translocation in endotoxemic rats. Sheng Li Ko Hsueh Chin Chan 1995;26:41-44.
34. Matsuyama Y, Morita T, Higuchi M, Tsujii T. The effect of taurine administration on patients with acute hepatitis. Prog Clin Biol Res 1983;125:461-468.
35. Ikeda H. Effects of taurine on alcohol withdrawal. Lancet 1977;2(8036):509.
36. Wilde MI, Wagstaff AJ. Acamprosate. A review of its pharmacology and clinical potential in the management of alcohol dependence after detoxification. Drugs 1997;53:1038-1053.
37. Sass H, Soyka M, Mann K, Zieglgansberger W. Relapse prevention by acamprosate. Results from a placebo-controlled study on alcohol dependence. Arch Gen Psychiatry 1996;53:673-680.
38. Whitworth AB, Fischer F, Lesch OM, et al. Comparison of acamprosate and placebo in long-term treatment of alcohol dependence. Lancet 1996;347:1438-1442.
39. Paille FM, Guelfi JD, Perkins AC, et al. Double-blind randomized multicentre trial of acamprosate in maintaining abstinence from alcohol. Alcohol Alcohol 1995;30:239-247.
40. Bara M, Guiet-Bara A, Durlach J, Pechery C. Comparative studies of Ca N-acetylhomotaurinate and Ca N-acetyltaurinate. I. Effects on the ionic transfer through the isolated human amnion. Methods Find Exp Clin Pharmacol 1995;17:233-240.
41. Guiet-Bara A, Bara M, Durlach J, Pechery C. Comparative studies of Ca N-acetylhomotaurinate and Ca N-acetyltaurinate. II. Preventive and opposing actions of the acute ethanol depletive effect on the ionic transfer through the isolated human amnion. Methods Find Exp Clin Pharmacol 1995;17:361-368.
42. Sturman JA. Nutritional taurine and central nervous system development. Ann NY Acad Sci 1986;477:196-213.
43. Airaksinen EM, Oja SS, Marnela KM, Sihvola P. Taurine and other amino acids of platelets and plasma in retinitis pigmentosa. Ann Clin Res 1980;12:52-54.
44. Uma SM, Satapathy M, Sitaramayya A. Decreased plasma taurine levels in retinitis pigmentosa. Biochem Med 1983;30:49-52.
45. Voaden MJ, Hussain AA, Chan IRP. Studies on retinitis pigmentosa in man. I. Taurine and blood platelets. Br J Ophthalmol 1982;66:771-775.
46. Reccia R, Pignalosa B, Grasso A, Campanella G. Taurine treatment in retinitis pigmentosa. Acta Neurologica 1980;18:132-136.
47. Fariello RG, Golden GT, McNeal RB Jr. Taurine and related amino acids in seizure disorders - current controversies. Prog Clin Biol Res 1985;179:413-424.
48. Airaksinen EM, Oja SS, Marnela KM, et al. Effects of taurine treatment on epileptic patients. Prog Clin Biol Res 1980;39:157-166.
49. Barbeau A, Inoue N, Tsukada Y, Butterworth RF. The neuropharmacology of taurine. Life Sci 1975;17:669-678.
50. Bergamini L, Mutani R, Delsedime M, Durelli L. First clinical experience on the antiepileptic action of taurine. Eur Neurol 1974;11:261-269.
51. Konig P, Kriechbaum G, Presslich O, et al. Orally-administered taurine in therapy-resistant epilepsy. Wien Klin Wochenschr 1977;89:111-113.
52. Marchesi GF, Quattrini A, Scarpino O, Dellantonio R. Therapeutic effects of taurine in epilepsy: a clinical and polyphysiographic study. Riv Patol Nerv Ment 1975;96:166-184.
53. Mongiovi A. Clinical study on the control of epilepsy using taurine. Riv Neurol 1978;48:305-325.
54. Takahashi R, Nakane Y. Clinical trial of taurine in epilepsy. In: Barbeau A, Huxtable RJ, eds. Taurine and Neurological Disorders. New York:Raven Press;1978:375.
55. Van Gelder NM, Sherwin AL, Sacks C, Anderman F. Biochemical observations following administration of taurine to patients with epilepsy. Brain Res 1975;94:297-306.
56. Mantovani J, DeVivo DC. Effects of taurine on seizures and growth hormone release in epileptic patients. Arch Neurol 1979;36:672-674.
57. Alder JT, Chessell IP, Bowen DM. A neurochemical approach for studying response to acetylcholine in Alzheimer's disease. Neurochem Res 1995;20:769-771.
58. Tomaszewski A, Kleinrok A, Zackiewicz A, et al. Effect of various amino acids on acetylcholine metabolism in brain tissue. Ann Univ Mariae Curie Sklodowska 1982;37:61-70.
59. Csernansky JG, Bardgett ME, Sheline YI, et al. CSF excitatory amino acids and severity of illness in Alzheimer's disease. Neurology 1996;46:1715-1720.
60. Franconi F, Bennardini F, Mattana A, et al. Plasma and platelet taurine are reduced in subjects with insulin-dependent diabetes mellitus: effects of taurine supplementation. Am J Clin Nutr 1995;61:1115-1119
The following was part of "cocksucker" thread, posted by Animal.
Taurine
Taurine, a sulfur containing amino acid derived from the amino acid cystine, is a component of the bile salts produced in the liver (it was first isolated from ox bile). It is important for proper digestion of fats and absorption of fat soluble vitamins. But only a fraction of available taurine is used to make bile salts,2 while an enormous amount floats freely inside cells.
Taurine is not incorporated into proteins but remains free in the tissues, especially muscle and nerve tissues. It has a number of therapeutic uses including acting as a membrane stabilizer and reducing arrhythmias of the heart. Taurine also enhances the contractile strength of heart muscle (called a positive inotropic effect)3, and thus can help treat heart failure which is a decreased ability of the heart to pump out all the blood that flows into it. When the heart is failing, the blood backs up and forces fluid out into the tissues (edema) by osmosis. This leads to either swelling of the legs or fluid in the lungs and shortness of breath, depending on which part of the heart is more involved.
In a 1984 animal study, taurine protected against heart failure, reducing mortality by 80 percent in the taurine treated group with no diminishment of cardiac function.4 In a later animal study in 1988, taurine was shown to lower blood pressure.5 My own clinical experience confirms some of these effects of taurine, and I commonly give it to patients with heart failure and high blood pressure.
Taurine is also beneficial for the eyes enhancing the rods and cones (the pigmented epithelial cells in the retina of the eye that serve as visual receptor cells). The greatest visual acuity occurs in the macular area of the retina near where the optic nerve enters from the back of the eye. With aging, the macula commonly degenerates as rods and cones die, often causing blindness. What causes the degeneration is not clear, but it is more common in diabetics and may be the result of free radical damage from ultraviolet light or oxygen exposure.6
A review of animal studies reveals that taurine appears to protect the eyes from macular degeneration.7 In one 1975 research report, a diet deficient in taurine was associated with retinal degeneration in cats.8 Thus, taurine can be part of a comprehensive approach to macular degeneration that also includes antioxidant nutrients, minerals, flavonoids, botanicals and chelation therapy (an intravenous therapy done in a doctor's office).
Because taurine is a neuroinhibitory amino acid, it may help treat seizure disorders. Some animal studies have suggested a role for taurine in controlling seizures, but the results are not consistent. In 1977, a cat with chronic epileptic seizures was successfully treated with taurine both orally and intravenously.9 Other studies have also suggested taurine's supportive role for seizures, but some clinical trials have shown limited benefits or have not confirmed this effect of taurine. I have used
taurine, in combination with magnesium and other nutrients, in my seizure patients with some success. It seems to enhance the effects of some of their seizure medications so they can take a lower dose.
REFERENCES
1. Linder, M., Ed. Nutritional Biochemistry and Metabolism, 2nd edition, Elsevier Scientific Publishing,
1991.
2. Chesney R.W. "Taurine: Its biological role and clinical implications," Adv Pediatr 32: 1 42, 1985.
3. Pisarenko, O.I. "Mechanisms of myocardial protection by amino acids: Facts and hypotheses," Clin Exp
Pharmacol Physiol 23(: 627 33, August, 1996.
4. Azuma, J., et al. "Beneficial effect of taurine on congestive heart failure induced by chronic aortic
regurgitation in rabbits," Res Commun Chem Pathol Pharmacol 45(2): 261 70, August, 1984.
5. Fujita, T., Sato, Y. "Hypotensive effect of taurine. Possible involvement of the sympathetic nervous system
and endogenous opiates," J Clin Invest 82(3): 993 97. September 1988.
6. Gaby, A.R., Wright, J.V. "Nutritional factors in degenerative eye disorders: Cataract and macular
degeneration," J Adv Med 6(1): 27 4O, Spring 1993.
7. Chesney, R.W. op. cit.
8. Hayes, K.C., Carey, R.E., et al. "Retinal degeneration associated with taurine deficiency in the cat,"
Science l88(4191): 949 51, May 30, 1975.
9. van Gelder, N.M., Koyama, I., et al. "Taurine treatment of spontaneous chronic epilepsy in a cat,"
Epilepsia 18(1): 45 54, March, 1977.
10. Pola, P., et al. "Statistical evaluation of long term L carnitine therapy in hyperlipoproteinaemias," Drugs
Exptl Clin Res 9: 925 34, 1983.
11. Orlando, G., Rusconi, C. "Oral L carnitine in the treatment of chronic cardiac ischaemia in elderly
patients," Clin Trials J 23: 338 44, 1986.
12. Singh, R.B., Niaz, M.A., et al. "A randomised, double blind, placebo controlled trial of L carnitine in
suspected acute myocardial infarction," Postgrad Med J 72(843): 45 50, January 1996.
13. Kobayashi, A., Watanabe, H., et al. "Effects of L carnitine and palmitoylcarnitine on membrane fluidity of
human erythrocytes," Biochim Biophys Acta 986(1): 83 8. Nov. 17, 1989.
14. Ghidini, O., Azzurro, M., et al. "Evaluation of the therapeutic efficacy of L carnitine in congestive heart
failure," Int J Clin Pharmacol Ther Toxicol 26(4): 217 20, April l988.
15. Dragan, I.G., Vasiliu A., et al. "Studies concerning chronic and acute effects of L carnitina in elite
athletes" Physiologie 26(2): 111 29, April June, 1989.
Taurine is the most abundant free amino acid in the brain, heart, and nervous system, and it plays a role in the normal functioning of the brain, heart, gallbladder, eyes, and vascular system. It facilitates the passage of sodium, potassium, and, possibly, calcium and magnesium, ions into and
out of cells, and electrically stabalizes cell membranes. It modulates the activity the activity of cAMP, which activates important enzymes in heary muscle, and contributes to the muscle's contractibility. Taurine is an important component of bile acids which aid in the absorption of fat soluble vitamins. It aids the body's chemistry by detoxifying harmful chemicals. Dietary taurine stimulates the formation of taurocholate, a substance which increases cholesterol secretion in the bile and also improves fat metabolism in the liver. Taurine offers a wide range of nutritional support to many organ systems throughout the body; as a supplement it is most notable known for
its heart muscle support.
Taurine induced NO production lowers cholesterol and dialtes veins too..
a few studies:
Quote:
Age-related progressive renal fibrosis in rats and its prevention with ACE inhibitors and taurine
Carmen Iglesias-De La Cruz1, Piedad Ruiz-Torres1, Raimundo Garcнa del Moral3, Manuel Rodrнguez-Puyol1, and Diego Rodrнguez-Puyol2,4
Departments of 1 Physiology and 2 Medicine, Alcalб University, Madrid; 3 Department of Pathology, Granada University, 18012 Granada; and 4 Nephrology Section, Hospital Prнncipe de Asturias, 28871 Alcalб de Heuares, Madrid, Spain
Our previous studies demonstrated an increased reactive oxygen species (ROS) production, as well as transforming growth factor-1 (TGF-1) expression in the rat kidney with aging. In the present study, we examined the effect of aging on extracellular matrix (ECM) accumulation and the effects of treatment with angiotensin-converting enzyme inhibitors (captopril and lisinopril) and taurine, an antioxidant amino acid. Age-related increases in types I and IV collagen and fibronectin mRNA expression were found at 24 and 30 mo of age. In contrast, type III collagen only increased in 30-mo-old rats. Captopril-, lisinopril-, and taurine-treated animals showed a statistically significant decrease in ECM protein expression at both ages. Moreover, treatment with taurine reduced the TGF-1 mRNA levels in 24- and 30-mo-old rats by 40%. Taurine also completely blocked increases in type I and type IV collagen expression in mesangial cells in response to TGF-1. Our results demonstrate a protective role from both converting enzyme inhibitors and taurine in the age-related progressive renal sclerosis. In addition, taking into account that taurine is considered as an antioxidant amino acid, present data suggest a role for ROS in age-related progressive renal fibrosis, perhaps through interactions with the TGF-1 pathway.
Quote:
Inhibition of hypertension and salt intake by oral taurine treatment in hypertensive rats.
Abe M, Shibata K, Matsuda T, Furukawa T.
Department of Pharmacology, School of Medicine, Fukuoka University, Japan.
Effects of oral treatment with taurine on fluid intakes produced by renin were assessed in spontaneously hypertensive rats of the Okamoto strain (SHR). Renin injected into the preoptic area increased water intake and evoked salt (2.7% NaCl solution) intake, and angiotensin II injected into this area increased water intake, but not salt intake, in both SHR and control normotensive Wistar-Kyoto rats (WKY). The salt intake elicited by renin, but not water intake produced by renin or angiotensin II, was potentiated in SHR. These effects of renin and angiotensin II on fluid intakes were antagonized by previous administration of taurine or gamma-aminobutyric acid into the cerebral ventricles in both strains. When SHR received water containing 3% taurine from 32 to 105 days of age, development of hypertension was inhibited. Renin administered into the preoptic area at 105 days of age caused an increase in salt intake, but the increase was markedly inhibited by the oral administration of taurine as well. These results show that salt appetite produced by centrally administered renin is exaggerated in SHR and that development of hypertension as well as renin-induced salt appetite in SHR is inhibited by dietary taurine.
Quote:
Taurine ameliorates chronic streptozocin-induced diabetic nephropathy in rats
H. Trachtman, S. Futterweit, J. Maesaka, C. Ma, E. Valderrama, A. Fuchs, A. A. Tarectecan, P. S. Rao, J. A. Sturman, T. H. Boles and al. et
Department of Pediatrics, Schneider Children's Hospital, Long Island Jewish Medical Center, Albert Einstein College of Medicine, New Hyde Park, New York 11040, USA.
We examined the effect of two endogenous antioxidant agents, taurine and vitamin E, on renal function in experimental diabetes. Male Sprague-Dawley rats, rendered diabetic with streptozocin (STZ), were assigned to one of the following groups: 1) untreated; 2) insulin treatment with 6 U Ultralente insulin/day in two doses; 3) taurine supplementation by 1% taurine in drinking water; and 4) vitamin E supplementation at 100 IU vitamin E/kg chow. Animals were kept for 52 wk. The survival rate was similar (70-90%) in all groups except vitamin E-treated animals, of which 84% died by 6 mo. At 52 wk, glomerular filtration rate was elevated in untreated and taurine-treated STZ rats compared with normal or insulin-treated diabetic rats. Taurine supplementation reduced total proteinuria and albuminuria by nearly 50%. This treatment also prevented glomerular hypertrophy, preserved immunohistochemical staining for type IV collagen in glomeruli, and diminished glomerulosclerosis and tubulointerstitial fibrosis in diabetic animals. The changes in renal function and structure in taurine-treated diabetic rats were associated with normalization of renal cortical malondialdehyde content, lowering of serum free Fe2+ concentration, and decreased formation of the advanced glycooxidation products, pentosidine, and fluorescence in skin collagen. Administration of the vitamin E-enriched diet exacerbated the nephropathy in STZ-diabetic rats. In addition, vitamin E supplementation increased serum free Fe2+ concentration, enhanced renal lipid peroxidation, and accelerated the accumulation of advanced glycosylation end products (AGEs) in skin collagen. We conclude that administration of taurine, but not vitamin E, to rats with STZ-diabetes ameliorates diabetic nephropathy. The beneficial effect of taurine is related to reduced renal oxidant injury with decreased lipid peroxidation and less accumulation of AGEs within the kidney.
Default
Taurine is a two-carbon, beta-amino acid, β-aminoethylsulfonic acid. Since taurine is not found in animal proteins, synthesis by the body is crucial. Taurine is synthesized from cysteine, and the conversion requires vitamin B6 (Figure 4-11). High plasma taurine is found associated with various stress reactions [86], apparently mediated by release of interleukin [87]. Increased plasma taurine is found in patients suffering from episodic acute psychosis characterized by sensory perceptual distortions. In such patients, oral loading with either serine or glycine can induce psychedelic symptoms [5]. The higher plasma taurine level in serineresponsive patients is caused by an increased synthesis of taurine from homocysteine and serine. Higher plasma taurine values are part of a pattern of amino acids associated with major depression [60]. Lower plasma glycine values and a higher serine/glycine ratio are found in depressed individuals. Depression is accompanied by decreasedexcitatory amino acids (e.g., glutamate), and increased inhibitory amino acids (e.g., taurine). A high plasma level can indicate excessiveproduction of taurine due to an inflammatory process mediated by white blood cells.
Taurine is found in high concentrations in heart muscle and white blood cells. Taurine is involved in mediation of chemical oxidation by white blood cell phagocytes in response to respiratory burst activity. Low or low normal cystine may indicate rapid conversion to taurine. Inadequate taurine supplies allow the oxidative activity to go unchecked, leading to excess oxidative damage and formation of aldehydes. Individuals with this condition are allergy-prone and often extremely sensitive to environmental chemicals. Taurine in the form of taurocholic acid is a key component of bile. Low taurine may accompany fat digestion problems [157], fatsoluble vitamin deficiencies, and high serum cholesterol levels [158]. Heart and brain cells require taurine for intracellular retention of calcium, magnesium, and potassium. Taurine has been used successfully in the treatment of congestive heart failure and is implicated in night blindness, arrhythmia, angina, hypercholesterolemia, and atherosclerosis [88]. Taurine deficiencies have been implicated in both neurological (epilepsy) and cardiovascular dysfunction. Beta-agonist drugs cause a reduction in the body pool of taurine [89, 90]. Choline supplementation may stimulate taurine synthesis due to its methyl-donator sparing function on methionine, thus freeing methionine for taurine biosynthesis [91]. Taurine also stabilizes platelets against aggregation. Platelets from taurine-depleted animals are twice as sensitive to aggregation as platelets from those receiving taurine. In addition, human subjects with normal taurine status show increased resistance to platelet aggregation by 30 or 70% when supplemented with taurine at 400 or 1600 mg/d, respectively [92]. Plasma taurine is easily raised by dietary supplementation. Concurrent low cysteine is also relevant in taurine depletion. Cysteine addition to formulas used for home parenteral nutrition normalizes plasma taurine concentrations in children with short gut syndrome [159]. - Citation :
- Concernant l'arginine, il semble qu'elle existe sous 2 formes: L-Arginine et Arginine AKG. On m'a dit que la forme A-AKG etait plus bio-disponible, serait-elle aussi plus efficace dans le cadre d'un programme d'exercice physique?
Oui, et oui. Mais différence difficilement mesurable...
D'autre part, il semble qu'il faille prendre entre 5 gr et 10 gr/ jour , les jours d'entrainement, pour pouvoir bénéficier de tous ces bienfaits (vasodilation+ stimulation raisonnable de l'hormone de croissance).
Sous quelle forme recommandez-vous l'arginine?
On m'a aussi dit qu'associé à la L-citrulline et la L-taurine, son role dans l'augmentation de l'oxyde nitrique est optimisée, qu'en pensez-vous?
Justement, prend plutôt de la citrulline malate : très nettement + efficace comme booster de No2 (pour moi en tt cas). La taurine a d'autres utilités pour ma part
Dans quel proportion faudrait-il associer l'arginine et les autres acides aminés?
Quel que soit ton sport, s'il est effectué avec intensité, l'idéal est de prendre de la béta alanine avant l'entrainement pour prévenir la dégradation musculaire (environ 5g si pris en 1 fois) et de la leucine de suite après l'entrainement. Les 2 fois avec des proteines, surtout si tu effectues un entrainement avec poids (environ 20 à 30g avant, et 30 à 40g après. Ou bien au minimum 15g de BCAA, mais c'est difficilement réalisable (goût infect si en poudre, prix...)
La simple prise de béta alanine atténue considérablement les courbatures, et la leucine est un anabolisant naturel (stimule la synthèse proteique).
Si tu prend de la béta alanine, évite la prise de taurine dans les 4h qui précèdent ou qui suivent, car il y a une compétition d'absorption entre ces 2 acides aminés dans l'organisme. La taurine en elle même est un supplément remarquable, mais je l'utilise plus pour aider à l'endormissement (le soir), normaliser le rythme cardiaque et pour aider à éliminer les déchets toxiques produits par l'organisme après un entrainement intense (plus jamais de courbatures. Dose : 5g également | |
|
Play-Fitness.fr 
Accueil 
