Taurine alters respiratory gas exchange and nutrient metabolism in type 2 diabetic rats

OBJECTIVE: To assess the effect of taurine supplementation on respiratory gas exchange, which might reflect the improved metabolism of glucose and/or lipid in the type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. RESEARCH METHODS AND PROCEDURES: Male OLETF rats (16 weeks of age) were randomly divided into two groups: unsupplemented group and taurine-supplemented (3% in drinking water) group. After 9 weeks of treatment, indirect calorimetry and insulin tolerance tests were conducted. The amounts of visceral fat pads, tissue glycogen, the blood concentrations of glucose, triacylglycerol, taurine, and electrolytes, and the level of hematocrit were compared between groups. A nondiabetic rat strain (Long-Evans Tokushima Otsuka) was used as the age-matched normal control. RESULTS: The indirect calorimetry showed that the treatment of OLETF rats with taurine could reduce a part of postprandial glucose oxidation possibly responsible for the increase of triacylglycerol synthesis in the body. Taurine supplementation also improved hyperglycemia and insulin resistance and increased muscle glycogen content in the OLETF rats. Supplementation with taurine increased the blood concentration of taurine and electrolyte and fluid volume, all of which were considered to be related to the improvement of metabolic disturbance in OLETF rats. DISCUSSION: Taurine supplementation may be an effective treatment for glucose intolerance and fat/lipid accumulation observed in type 2 diabetes associated with obesity. These metabolic changes might be ascribed, in part, to the alteration of circulating blood profiles, where the improved hyperglycemia and/or the blood accumulation of taurine itself would play roles.     

Taurine improves insulin sensitivity in the Otsuka Long-Evans Tokushima Fatty rat, a model of spontaneous type 2 diabetes

BACKGROUND: Taurine, a potent antioxidant, has been reported to improve streptozotocin-induced diabetes mellitus, in which the development of diabetes results from an attack by oxygen free radicals on pancreatic beta cells. However, taurine also increases the excretion of cholesterol via conversion to bile acid and would be expected to improve insulin resistance. OBJECTIVE: The effects of taurine on insulin sensitivity were examined in a model rat of insulin resistance and type 2 diabetes-the Otsuka Long-Evans Tokushima Fatty (OLETF) rat. DESIGN: Male OLETF rats were divided into 2 groups at the age of 16 wk: a taurine-supplemented group and an unsupplemented group. As a nondiabetic control, Long-Evans-Tokushima-Otsuka rats were used. An oral-glucose-tolerance test and hyperinsulinemic euglycemic clamp were performed at the ages of 23 and 25 wk. RESULTS: The OLETF rats had hyperglycemia and insulin resistance and they had a greater accumulation of abdominal fat than did control rats. Abdominal fat accumulation, hyperglycemia, and insulin resistance were significantly lower in the taurine-supplemented group than in the unsupplemented group. Serum and liver concentrations of triacylglycerol and cholesterol were significantly higher in the OLETF rats than in the control rats and were significantly lower in the taurine-supplemented group than in the unsupplemented group, presumably because of the increased secretion of cholesterol into bile acid. Taurine-supplemented rats also showed higher nitric oxide secretion, evidenced by increased urinary excretion of nitrite. CONCLUSION: Taurine effectively improves metabolism in OLETF rats by decreasing serum cholesterol and triacylglycerol, presumably via increased secretion of cholesterol into bile acid and decreased production of cholesterol because of increased nitric oxide production.     

Differential regulation of the degradation of myofibrillar and total proteins in skeletal muscle of rats: effects of streptozotocin-induced diabetes, dietary protein and starvation

In order to examine the effects of streptozotocin-induced diabetes, dietary protein, and starvation on protein degradation in skeletal muscle of perfused rat hindquarters, rates of myofibrillar and total protein degradation were estimated from the release of 3-methylhistidine (N tau-methylhistidine, 3-MH) and tyrosine, respectively. In rats fed a 20% protein diet (controls), the fractional degradation rate of myofibrillar protein was approximately 56% of the total muscle protein. In streptozotocin-induced diabetic rats, 3-MH release by perfused muscle increased significantly on d 1 of treatment and sustained a high level thereafter. By contrast, tyrosine release did not change. Feeding a 50% protein diet for 1 wk altered neither 3-MH nor tyrosine release. Protein-free feeding, though, suppressed tyrosine release to 49% of controls, but did not affect 3-MH release. Starvation for 3 d did not affect tyrosine release, but did increase 3-MH release to 203% of controls. These results indicate that in diabetic and starved rats myofibrillar protein is preferentially degraded, while in protein-deficient rats, non-myofibrillar protein degradation is selectively suppressed. From these observations, we conclude that the degradation of myofibrillar and non-myofibrillar proteins in skeletal muscle can be differentially regulated.     

Dietary taurine alters ascorbic acid metabolism in rats fed diets containing polychlorinated biphenyls

The effect of dietary taurine on ascorbic acid metabolism and hepatic drug-metabolizing enzymes was investigated in rats fed diets containing polychlorinated biphenyls (PCB) to determine whether taurine has an adaptive and protective function in xenobiotic-treated animals. Young male Wistar rats (60 g) were fed diets containing 0 or 0.2 g/kg diet PCB with or without 30 g/kg diet of taurine for 14 d. The rats fed the PCB-containing diets had greater liver weight, higher ascorbic acid concentrations in the liver and spleen and greater hepatic cytochrome P-450 contents than control rats that were not treated with PCB (P < 0.01). In PCB-fed rats, urinary ascorbic acid excretion was enhanced, and serum cholesterol concentration (especially HDL-cholesterol) was significantly elevated compared with those in control rats. Dietary taurine significantly potentiated the increases in the urinary excretion of ascorbic acid and the rise in the levels of cytochrome P-450 which were caused by PCB treatment. On the other hand, the supplementation of taurine to control diet did not alter these variables. Taurine may enhance the hepatic drug-metabolizing systems, leading to the stimulation of the ascorbic acid metabolism in rats fed diets containing PCB.     

Antioxidant effect of taurine against lead-induced oxidative stress

Oxidative stress is proposed as a molecular mechanism in lead toxicity, which suggests that antioxidants might play a role in the treatment of lead poisoning. The present study was designed to investigate whether taurine has a beneficial effect both on Chinese hamster ovary (CHO) cells and on Fisher 344 (F344) rats following lead exposure. Therefore, oxidative stress parameters (glutathione, malondialdehyde levels, catalase, and glucose-6-phosphate dehydrogenase [G6PD] activities) of lead-exposed CHO cells and F344 rats were determined following taurine treatment. Taurine was found to be effective in (1) increasing glutathione levels that had been diminished by lead; (2) reducing malondialdehyde levels, an end-product of lipid peroxidation; (3) decreasing catalase and erythrocyte G6PD activity, which had been increased by lead exposure; and (4) improving cell survival of CHO cells. However, taurine had no effect on blood and tissue lead levels when 1.1 g/kg/day taurine was administered to F344 rats for 7 days, following 5 weeks of lead exposure (2,000 ppm lead acetate). As a result, taurine seems to be capable of fortifying cells against lead-induced oxidative attack without decreasing lead levels. Therefore, administration of taurine, accompanied by a chelating agent, might increase its effectiveness in the treatment of lead poisoning. Received: 30 January 2001/Accepted: 11 May 2001     

Effects of insulin, amino acids and fasting on myofibrillar protein degradation in perfused hindquarters of rats

The rate of 3-methylhistidine (3-MH) release from rat perfused hindquarters was measured to investigate the effects of insulin, amino acids and fasting on myofibrillar protein degradation. Since release of 3-MH into the perfusate increased linearly and the pool of free 3-MH in the perfused muscle did not change significantly during 2 h of perfusion, it was concluded that 3-MH release reflected the rate of myofibrillar protein degradation. Tyrosine release in the presence of cycloheximide represented the degradation rate of total muscle protein. Insulin suppressed the net release of tyrosine in normal rats, but did not affect the rate of release of 3-MH and tyrosine in the presence of cycloheximide. 3-MH release was not influenced by perfusate amino acid concentrations at zero to 5 times the normal plasma levels. When rats were fasted for one and two days, 3-MH release increased 1.7 and 2.6 times, respectively, compared with the fed rats, which showed that the rate of degradation of myofibrillar protein in skeletal muscle rose just after the beginning of fasting.     

牛磺酸对大鼠酒精性肝损伤保护作用的研究

目的 :　通过观察牛磺酸对大鼠酒精性肝损伤的保护效果 ,为预防及治疗酒精性肝损伤提供理论及实验依据。方法 :　通过白酒灌胃建立大鼠酒精性肝损伤模型 ,治疗组分别给予高低两种剂量的牛磺酸 ,对照组 0 .9%生理盐水 ,实验末测血压、血清甘油三酯 (TG) ,并对大鼠肝脏进行病理及量化分析。结果 :　与模型组相比 ,高低两种浓度的 (2 %和 5 %)牛磺酸均可以显著降低酒精性肝损伤大鼠血清甘油三酯 (P<0 .0 5 ) ;高剂量组牛磺酸还能降低酒精性肝损伤大鼠血压(P<0 .0 5 ) ;肝脏病理切片量化分析显示 ,高低两种剂量牛磺酸均可显著降低酒精对肝脏的损伤 (P<0 .0 5 ) ,且高低剂量组的保护效果无显著性差异 (P>0 .0 5 )。结论 :　牛磺酸能够有效保护酒精对大鼠肝脏的损伤。     

Lipid peroxidation potential and antioxidants in the heart tissue of beta-alanine- or taurine-treated old rats

The aim of this study was to investigate the effect of the changes of taurine levels in the hearts of old rats on endogenous malondialdehyde (MDA) and diene conjugate (DC) levels and ascorbic acid (AA)- and NADPH-induced lipid peroxidation as well as non-enzymatic (glutathione, vitamin E and vitamin C) and enzymatic antioxidants (superoxide dismutase, glutathione peroxidase and glutathione transferase). Two groups of old (22 mo) rats were treated with beta-alanine (3%, w/v; in drinking water), a taurine depleting agent, or taurine (2% w/v; in drinking water) for 6 wk. Significant decreases were observed in taurine contents of hearts in old rats as compared to young (5 mo) rats. We found that MDA and DC levels and AA- and NADPH-induced lipid peroxidation increased, but non-enzymatic and enzymatic antioxidants did not alter in heart homogenates of aged rats. beta-Alanine administration resulted in significant decreases in heart taurine levels of old rats. This treatment did not cause further increases in MDA or DC levels or changes in antioxidants. However, AA- and NADPH-induced lipid peroxidation was higher than that of old rats. Taurine treatment caused significant increases in heart taurine levels of old rats. This treatment was found to decrease endogenous MDA and DC levels without affecting the antioxidant system in the heart homogenates of aged rats. AA- and NADPH-induced lipid peroxidation was also reduced in old rats when given taurine, although not statistically significantly. Our results indicate that the changes in heart taurine levels may influence the susceptibility of heart tissue to lipid peroxidation in aged rats and that taurine supplementation has protective effects on age-dependent oxidative stress in heart tissue.     

Effect of dietary taurine on plasma and blood cell taurine concentrations in cats

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

Dietary soya protein intake and exercise training have an additive effect on skeletal muscle fatty acid oxidation enzyme activities and mRNA levels in rats

Exercise training and regular physical activity increase oxidation of fat. Enhanced oxidation of fat is important for preventing lifestyle diseases such as hypertension and obesity. The aim of the present study in rats was to determine whether intake of dietary soya protein and exercise training have an additive effect on the activity and mRNA expression of enzymes involved in skeletal muscle fatty acid oxidation. Male Sprague-Dawley rats (n 32) were assigned randomly into four groups (eight rats per group) and then divided further into sedentary or exercise-trained groups fed either casein or soya protein diets. Rats in the exercise groups were trained for 2 weeks by swimming for 120 min/d, 6 d/week. Exercise training decreased hepatic triacylglycerol levels and retroperitoneal adipose tissue weight and increased skeletal muscle carnitine palmitoyltransferase 1 (CPT1) activity and mRNA expression of CPT1, beta-hydroxyacyl-CoA dehydrogenase (HAD), acyl-CoA oxidase, PPARgamma coactivator 1alpha (PGC1alpha) and PPARalpha. Soya protein significantly decreased hepatic triacylglycerol levels and epididymal adipose tissue weight and increased skeletal muscle CPT1 activity and CPT1, HAD, acyl-CoA oxidase, medium-chain acyl-CoA dehydrogenase, PGC1alpha and PPARalpha mRNA levels. Furthermore, skeletal muscle HAD activity was the highest in exercise-trained rats fed soya protein. We conclude that exercise training and soya protein intake have an important additive role on induction of PPAR pathways, leading to increased activity and mRNA expression of enzymes involved in fatty acid oxidation in skeletal muscle and reduced accumulation of body fat.     

牛磺酸对不同龄雄性大鼠性功能的影响

目的:研究牛磺酸对不同龄雄性大鼠性功能的影响。方法:通过在青年和老年雄性大鼠饮水中添加牛磺酸和β-丙氨酸(牛磺酸转运抑制剂)30天后,进行阴茎勃起实验和交配实验观测。结果:牛磺酸对青年大鼠勃起次数、勃起潜伏期、乘骑次数、插入次数、射精次数、捕捉潜伏期均没有影响,但可显著提高老年大鼠勃起次数、乘骑次数、射精次数,明显缩短勃起潜伏期和捕捉潜伏期。结论:牛磺酸对维持雄大鼠正常的性功能具有重要作用,并可增强老年雄性大鼠的性功能。     

Hypertaurinemia in bile duct-ligated rats after surgery: the effect of gut endotoxin restriction on organ fluxes and oxidative status

Surgery in obstructive jaundice is associated with complications related to gut-derived endotoxemia. The organs involved in these complications, including liver, kidneys, and gut, are important in the metabolism of taurine, which is implicated in bile acid conjugation and has antioxidative effects. Taurine organ metabolism and liver oxidative status were studied in bile duct-ligated rats (BDL) after laparotomy. Oral cholestyramine treatment inhibits gut-derived endotoxemia and was used to evaluate the role of endotoxin. In BDL rats, postoperative plasma taurine levels were higher compared with SHAM (p < .0001). Cholestyramine treatment reduced plasma taurine in BDL rats (p < .005), but levels remained higher compared with SHAM groups (p < .0001). In contrast to a liver uptake of taurine in SHAM rats, a release from livers of BDL rats was found (p < .005). Cholestyramine treatment in BDL rats resulted in a liver uptake of taurine (p < .05 vs BDL). A higher uptake of taurine by the kidneys was found in both BDL animals after surgery and SHAM controls (p < .005); however, cholestyramine had no effect. A release of taurine from the gut was found in the SHAM groups, which was reversed in both BDL groups (p < .01). Cholestyramine lowered the elevated levels of hepatic enzymes in BDL rats (ALT and AST: p < .05). Total liver glutathione levels were lower in BDL rats (p < .0001) compared with SHAM groups, and cholestyramine significantly attenuated this decrease (p < .01). Liver malondialdehyde levels were higher in BDL rats compared with SHAM (p < .01), whereas cholestyramine completely prevented this increase in lipid peroxidation (p < .0001). Hypertaurinemia in BDL rats after surgery is most likely explained by reduced bile acid conjugation and hepatocellular leakage. Cholestyramine treatment reduced hepatocellular damage by inhibiting gut-derived endotoxemia, and reversed the release of taurine from the jaundiced liver into an uptake and consequently lowered plasma taurine levels. This uptake may contribute to the improved antioxidant status in cholestyramine-treated BDL rats.     

The effects of starvation and refeeding on muscle protein synthesis and catabolism in the young rat

We studied the effects of acute starvation and refeeding on muscle protein synthesis and degradation in young rats. As measures of synthesis, we determined muscle RNA concentration and the rate of incorporation of [14C]leucine into skeletal muscle protein (Sm). As an estimate of nitrogen retention we measured urea production (UrP). Starvation reduced these variables significantly. One refeeding period returned Sm to control values, only partially restored RNA concentration, and increased UrP. We determined the urinary excretion rate of 3-methylhistidine (3-MH) as a measure of the rate of myofibrillar protein degradation. Excretion of 3-MH was lowest in control and highest in starved rats. Refeeding decreased 3-MH excretion to a level midway between control and starved animals. Growth was attended by high rates of synthesis and low rates of degradation. Starvation depressed synthesis and increased degradation. With refeeding, synthesis increased and degradation decreased, compared with the starved state.     

The effect of taurine on the cholesterol metabolism in rats fed diets supplemented with cholestyramine or high amounts of bile acid

The effects of taurine on serum cholesterol levels and hepatic cholesterol 7alpha-hydroxylase activity (CYP7A1) were studied in rats fed cholestyramine or high amounts of sodium cholate in order to alter the intestinal pool of bile acids. Rats were fed a diet supplemented with 1% cholesterol and 0.25% sodium cholate (high cholesterol, control; C), and C supplemented with 4% cholestyramine (CH) or 0.75% sodium cholate (BA) for 14 d. Taurine groups were fed the diet supplemented with 3% taurine (CT, CHT and BAT). Compared to rats fed C and BA diets, serum cholesterol levels were significantly reduced in rats fed CT and BAT diets, but a significant reduction of serum cholesterol by taurine feeding was not observed in the CHT group as compared to the CH group. An increase in hepatic CYP7A1 activity due to taurine intake was observed in the CT and BAT groups. However, the simultaneous administration of cholestyramine and taurine (CHT group) did not increase hepatic CYP7A1 activity compared the intake of cholestyramine only (CH group). A significant increase in fecal bile acid excretion due to taurine intake was found only in rats fed the CT diet. In conclusion, it is suggested that taurine facilitates hepatic CYP7A1 activity regardless of the enlarged intestinal pool of bile acids due to increased intake of exogenous bile acid, and then reduces the serum cholesterol concentration.     

Effects of taurine on plasma and liver lipids, erythrocyte ouabain sensitive Na efflux and platelet aggregation in Sprague Dawley rats

The effects of taurine on plasma and liver cholesterol, erythrocyte ouabain sensitive Na efflux and platelet aggregation were examined in Sprague Dawley rats fed control or 0.5% cholesterol with 0.2% cholate diet. Plasma and liver levels of total cholesterol were increased significantly (p<0.05) in rats fed cholesterol diet compared to the control, and taurine significantly decreased the elevated plasma level of cholesterol in rats fed cholesterol diet (p<0.05). HDL-cholesterol was decreased in groups fed the cholesterol diet regardless of taurine supplementation and the difference between groups with and without cholesterol was significant (p<0.01). Plasma triglyceride was decreased and liver triglyceride was increased both significantly (p<0.05) in rats fed cholesterol compared to the control. Plasma and liver triglyceride in rats fed taurine was decreased significantly compared to the control (p<0.05). Intracellular Na tended to be lower in rats fed cholesterol or taurine and higher in rats fed cholesterol plus taurine compared to the control. Na efflux through Na-K ATPase and the passive leak of Na was somewhat reduced in rats fed cholesterol or taurine and was augmented in rats fed cholesterol plus taurine compared to the control, which showed a similar trend to the intracellular Na. Taurine supplementation caused a suppression of Na efflux in groups fed control diet and restored the suppressed Na efflux in groups fed cholesterol. Platelet aggregation was significantly decreased in the group fed taurine compared to the control (p<0.05) and the group fed cholesterol plus taurine was also a little lower in aggregation than the group fed cholesterol. Microscopic examination showed that taurine prevented fatty liver in rats fed cholesterol diet. Taurine known for stimulating Na-K ATPase in some cell types rather decreased erythrocyte ouabain sensitive Na-K ATPase in the present study. Taurine had hypolipidemic and hypocholesterolemic effects and inhibited platelet aggregation which may be favorable for prevention of cardiovascular diseases.     

牛磺酸对铅中毒大鼠红细胞免疫功能损伤的治疗作用

目的　了解牛磺酸对铅中毒大鼠红细胞免疫功能的影响。方法　把30只Wistar大鼠随机分为正常对照组、铅染毒对照组、治疗组,每组10只动物。对照组用蒸馏水灌胃,其余组用6 g/L醋酸铅溶液按每次60 mg/kg灌胃;染毒30 d后,治疗组动物用400 mg/kg的牛磺酸每天灌胃1次,正常对照组及铅染毒对照组用等剂量蒸馏水灌胃,连续30 d。采用酵母菌花环试验测定红细胞C3b受体花环率(RBC- C3b -RR)和红细胞免疫复合物花环率(RBC- CIC -RR)。结果　染毒对照组RBC C3b RR明显低于正常对照组(P<0 .01),其RBC- CIC- RR明显高于正常对照组(P<0 .01),治疗组的RBC- C3b- RR明显高于染毒组(P<0. 01),而其RBC CIC RR明显低于染毒组(P<0. 05)。结论　牛磺酸对铅中毒大鼠红细胞免疫功能的损伤具有明显的保护作用。     

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

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

牛磺酸对幼鼠脑神经保护作用和机制研究

目的　观察牛磺酸 (Tau)对幼鼠脑神经的保护作用 ,并对其可能机制进行探讨。方法　用 0 .1 μmol/L亚硒酸钠与不同浓度的 Tau共同加入到原代培养 2 d的新生小鼠大脑皮质神经元中 ,用 MTT检测和 DNA片段琼脂糖凝胶电泳法分析其保护性作用 ;并选用健康清洁级、断乳SD雌鼠 3 2只 ,按体重随机分为 4组 ,分别饲予补充不同水平 Tau的实验饲料 ,观察对照组及补充Tau组幼鼠脑发育及代谢的影响。结果　 1 .Tau可明显提高神经元的存活率 ;2 .一定浓度的 Tau可阻断或部分阻断由亚硒酸钠诱导的典型 DNA梯型 ;3 .Tau可促进脑细胞的增殖活性 ,增加脑重 ;4.补充 Tau能明显提高脑 Tau积累、蛋白质和 ACh E水平 ,且有一定的剂量反应关系。结论　补充 Tau具有较强的神经保护作用 ,可能是通过改变某些蛋白质即某些基因的表达而实现的。     

Reversal of ethanol-induced hepatic steatosis and lipid peroxidation by taurine: a study in rats.

Alcohol (ethanol) was administered chronically to female Sprague-Dawley rats in a nutritionally adequate, totally liquid diet for 28 days. This resulted in significant hepatic steatosis and lipid peroxidation. When taurine was administered for 2 days following alcohol withdrawal it was found to reduce alcohol-induced lipid peroxidation and completely reversed hepatic steatosis. The reversal of hepatic steatosis was demonstrated both biochemically and histologically. Two days following alcohol withdrawal, the apparent activity of the alcohol-inducible form of cytochrome P450 (CYP2E1) was unchanged although total cytochrome P450 content was increased. In addition, alcohol significantly inhibited hepatic methionine synthase activity and increased homocysteine excretion in urine. Although alcohol did not affect the urinary excretion of taurine (a non-invasive marker of liver damage), levels of serum and hepatic taurine were markedly raised in animals given taurine following their treatment with alcohol, compared to animals given taurine alone. There was evidence of slight bile duct injury in animals treated with alcohol and with alcohol followed by taurine, as indicated by raised serum alkaline phosphatase (ALP) and cholesterol. Aspartate aminotransferase (AST) was also slightly raised. The effects of taurine on reversing hepatic steatosis may be due to the enhanced secretion of hepatic triglycerides. It is suggested that increased bile flow as a result of taurine treatment may have contributed to the removal of lipid peroxides. These in-vivo findings demonstrate for the first time that hepatic steatosis and lipid peroxidation, occurring as a result of chronic alcohol consumption, can be reversed by administration of taurine to rats for 2 days.