Effects Of Taurine Supplementation Research Articles

Lipid Metabolism and Peroxidation in Broiler Chicks under Chronic Heat Stress

The effects of taurine supplementation on growth performance, serum and liver concentrations of lipid, fatty acid composition and lipid peroxidation in the livers of broilers under chronic heat exposure conditions were investigated. The chicks with a similar body weight were equally assigned to one of three controlled-environment chambers. The brolier chicks, which were kept at 34°C were fed either with a control diet or the control diet supplemented with 0.8% taurine, whereas broiler chicks kept at 22°C were fed a control diet. Both of the BW and BW gains of broilers maintained at a temperature of 34°C were significantly lower than those of the control group, which was maintained at a temperature of 22°C (p<0.05). However, taurine addition in the diet of birds submitted to heat stress siginficantly improved BW gain (p<0.05). The feed intake of chicks declined with increases in temperature. The relative liver and gall bladder weights of chicks fed the control diet and maintained at 34°C were significantly lower than those measured in the control birds (p<0.05). However, dietary taurine was found to compensate for these reductions in liver and gall bladder weights. Relative weights of abdominal fat did not differ significantly among the three groups. Serum triglyceride concentrations were significantly lower in the chicks fed the control diet and maintained at 34°C compare to those measured in the chicks fed the control diet at 22°C (p<0.05). Heat stress resulted in a significant reduction in total lipid and triglyceride levels, but also increased the levels of total cholesterol in the liver (p<0.05). However, dietary taurine supplementation under the heat stress condition resulted in the recovery, to control levels, of serum triglyceride concentrations, as well as the amounts of total lipids, triglycerides, and cholesterol in the liver. The livers of chicks fed on taurine diets at 34°C showed significantly higher proportions of C14:0, C16:1, C18:1, C18:2, and 20:3, and lower C18:0 and C20:4 proportions than those of chicks fed on control diets at the same temperature (p<0.05). The total levels of saturated fatty acids decreased, but monounsaturated fatty acids and unsaturated fatty acid levels increased in chicks fed the taurine diet, as compared to chicks fed the control diet at 34°C (p<0.05). Peroxidizability indices were significantly lower in the heat-exposed chicks fed the taurine diet than in the non-taurine heat-exposed groups (p<0.05). In conclusion, dietary taurine results in an increase in the growth performances of chicks under heat stress conditions via improvements in lipid absorption and metabolism, as well as an induced reduction in lipid peroxidation.

Intestinal Failure–Associated Liver Disease: What Do We Know Today?

Intestinal failure-associated liver disease develops in 40% to 60% of infants who require long-term total parenteral nutrition (TPN) for intestinal failure and 15% to 40% of adults on home parenteral nutrition. The clinical spectrum includes hepatic steatosis, cholestasis, cholelithiasis, and hepatic fibrosis. Progression to biliary cirrhosis and the development of portal hypertension and liver failure occurs in a minority but is more common in infants and neonates than in adults. The pathogenesis is multifactorial. In infants it is related to prematurity, low birth weight, duration of PN, short bowel syndrome requiring multiple laparotomies, and recurrent sepsis. Other important mechanisms include lack of enteral feeding, which leads to reduced gut hormone secretion; reduction of bile flow and biliary stasis, which leads to the development of cholestasis; and biliary sludge and gallstones, which exacerbate hepatic dysfunction. In adults, IFALD is less common and related to age, length of time on PN, total caloric intake, and lipid or glucose overload. In preterm infants, a deficiency of taurine or cysteine may play a role, whereas in both adults and children, choline deficiency may exacerbate IFALD. Lipid emulsions, choline deficiency, and manganese toxicity are associated with both hepatic steatosis and cholestasis in adults and children. Management strategies for the prevention of intestinal failure-induced liver disease include early enteral feeding, a multidisciplinary approach to the management of parenteral nutrition, and aseptic catheter techniques to reduce sepsis. The addition of choline, taurine, and cysteine to PN solutions may also play a role. Oral administration of ursodeoxycholic acid may improve bile flow and reduce gallbladder stasis. Survival after either isolated small bowel or combined liver and small bowel transplantation is approximately 50% at 5 years, making this an acceptable therapeutic option in adults and children with irreversible liver and intestinal failure.

No effect of taurine on platelet aggregation in men with a predisposition to type 2 diabetes mellitus

AbbreviationsADP–denosine diphosphate; BMI–body mass index; FFA–free fatty acids; FFM–fat-free mass; IGT–impaired glucose tolerance; OGTT–oral glucose tolerance test; PPP–platelet-poor plasma; PRP–platelet-rich plasma; T2DM–type 2 diabetes mellitus; TG–triglyceride.Contributed equally to this study.Any diet therapy that potentially could affect platelet function would also influence the initiation of atherosclerotic plaque formation which is an important complication of diabetes mellitus eventually resulting in myocardial infarction and stroke. Blood platelets are rich in taurine, and it has been shown that taurine inhibits platelet aggregation in healthy subjects. The purpose was to examine the effect of taurine supplementation on platelet aggregation in high-risk subjects with a positive family history of T2DM. Twenty healthy men were included in a double-blinded, randomized, crossover study, receiving daily supplementation of 1.5 g taurine or placebo for two 8-week periods. Subjects were overweight and first-degree relatives of T2DM patients. At the end of each treatment, fasting blood samples for assessment of platelet aggregation was drawn. Platelet aggregation was induced by ADP. Plasma taurine concentration was significantly greater after taurine intervention compared to placebo (131.4 ± 61.7 vs. 38.9 ± 6.7 µmol/l, P < 0.0001). There was no difference in the threshold level for complete platelet aggregation induced by ADP in vivo between placebo and taurine intervention (placebo 3.86 ± 2.21 vs. taurine 3.86 ± 3.25 µmol/l). Supplementation with 1.5 g of taurine for 8 weeks had no effect on platelet aggregation in overweight prediabetic men.

식이내 타우린 첨가가 비육돈의 성장, 등지방두께, 체내 콜레스테롤 및 타우린 농도에 미치는 영향

식이내 타우린 첨가가 비육돈의 성장, 등지방두께, 체내 콜레스테롤 및 타우린 농도에 미치는 영향

Taurine renders the cell resistant to ischemia-induced injury in cultured neonatal rat cardiomyocytes.

Taurine is found in very high concentration in the mammalian heart. Because chronic myocardial taurine loss produces myocardial injury, the effects of taurine supplementation on ischemia-induced necrosis and apoptosis were examined using a cardiomyocyte model of simulated ischemia. Neonatal rat heart cells were cultured for 24-72 h in a sealed flask, a condition that leads to simulated ischemia characterized by a decrease in the pH and oxygen content of the medium and a catabolite accumulation. The consequences of altered medium taurine on cellular apoptosis and necrosis were then evaluated. Exposure of cardiomyocytes to medium containing high extracellular concentrations of taurine (20 mM) significantly elevated intracellular taurine levels, reduced p53 content, and enhanced cellular Bcl-2 content. In the absence of taurine treatment, simulated ischemia led to cellular release of creatine phosphokinase (CPK), morphologic degeneration, and beating cessation by 24-72 h. Based on DNA ladder analysis and the Hoechst 33258 staining pattern, a significant number of cells placed in sealed flasks underwent apoptosis. CPK was lost from some of the cells during simulated ischemia. In contrast to the untreated ischemic cells, the cells that were incubated in medium supplemented with taurine exhibited significantly less ischemia-induced necrosis and apoptosis. The data suggest that taurine renders the cell resistant to ischemia-induced necrosis and apoptosis. The beneficial effects of taurine may be related to the elevation in cellular Bcl-2 content.

Effect of taurine supplementation on the lipid peroxide formation and the activities of glutathione-related enzymes in the liver and islet of type I and II diabetic model mice.

Effects of taurine supplementation on lipid peroxide formation and the activities of glutathione (GSH) dependent enzymes in diabetic model mice were investigated. Type I diabetes mellitus was induced by injecting alloxan to ICR mice while type II diabetes mellitus was produced by high calorie diet feeding to genetically hyperglycemic KK mice. Taurine was given in drinking water at the level of 5% (w/v) for seven days. The malondialdehyde (MDA) levels of liver and the islets of type I diabetes were significantly increased compared to the control group but the levels were significantly decreased by taurine supplementation. In the type II diabetic model, the concentrations of MDA were not changed by taurine treatment. The activity of hepatic and islet GSH-peroxidase (GPX) was increased in the type I diabetic group, but in type II animals it was decreased. Hepatic GPX activity of both type I and II diabetics was not altered by taurine supplementation but was increased in the islets of the type II animals. No effect on the activity of GSH S-transferase (GST) was observed in both types of diabetes (I and II) following taurine supplementation. These results suggest that taurine supplementation protects type I diabetic mice from lipid peroxide formation.

Effects of taurine supplementation on lipid peroxidation, blood glucose and blood lipid metabolism in streptozotocin-induced diabetic rats.

The purpose of this study was to determine the effect of taurine on several complications of diabetes, including oxidative stress, glucose intolerance and blood lipid profile. Sprague Dawley male rats were fed an experimental diet for 7 weeks, at which time they were maintained on drinking water with or without 1% taurine. The experimental period was 7 weeks and the rats were administered streptozotocin (STZ) to induce diabetes. Thiobarbituric acid reactive substances (TBARS) content was increased following the STZ injection, but was lowered by prior treatment with taurine. The primary diabetic symptoms, such as polydipsia and polyuria, were ameliorated in rats supplemented with taurine before the STZ injection. Plasma triglyceride (TG) levels of the diabetic group were decreased by taurine supplementation, although plasma total cholesterol (T-chol) and HDL cholesterol (HDL-chol) were not different among the groups. LDL cholesterol (LDL-chol) levels of the control group were significantly decreased by taurine supplementation, however, the time of taurine administration affected the response of the diabetic group; only diabetic rats treated with taurine after the administration of STZ showed a decrease in LDL cholesterol. Therefore, taurine inhibits lipid peroxidation and decreases blood TG and LDL-chol levels, however, the time and dose of taurine supplementation are variables that need to be considered in the treatment of diabetes.

Plasma and whole blood taurine concentrations respond differently to taurine supplementation (humans) and depletion (cats)

In the present study the relationship between plasma and whole blood taurine was examined under normal physiological circumstances in humans and cats. In addition, the effect of taurine supplementation on plasma and whole blood taurine was evaluated in humans and the depletion of taurine pools after a taurine-deprived diet was studied in cats. The normal plasma taurine concentration in humans was 44 +/- 8 mumol/L and the whole blood taurine concentration was 227 +/- 35 mumol/L. Under normal physiological conditions plasma and whole blood taurine were not correlated (r = 0.092). Plasma taurine responded rapidly to dietary supplementation in humans or the taurine depletion in cats. In contrast, the whole blood taurine pool was more inert and varied only under extremes of depletion (cats) or sustained taurine supplementation.

Plasma and platelet taurine are reduced in subjects with insulin-dependent diabetes mellitus: effects of taurine supplementation

Plasma and platelet taurine concentrations were assayed in 39 patients with insulin-dependent diabetes mellitus (IDDM) and in 34 control subjects matched for age, sex, and both total and protein-derived daily energy intake. Platelet aggregation induced by arachidonic acid in vitro at baseline and after oral taurine supplementation (1.5 g/d) for 90 d was also studied. Plasma and platelet taurine concentrations (mean +/- SEM) were lower in diabetic patients (65.6 +/- 3.1 mumol/L, or 0.66 +/- 0.07 mol/g protein) than in control subjects (93.3 +/- 6.3 mumol/L, or 0.99 +/- 0.16 mol/g protein, P < 0.01). After oral supplementation, both plasma and platelet taurine concentrations increased significantly in the diabetic patients, reaching the mean values of healthy control subjects. The effective dose (mean +/- SEM) of arachidonic acid required for platelets to aggregate was significantly lower in diabetic patients than in control subjects (0.44 +/- 0.07 mmol compared with 0.77 +/- 0.02 mmol, P < 0.001, whereas after taurine supplementation it equaled the mean value for healthy control subjects (0.72 +/- 0.04 mmol). In in vitro experiments, taurine reduced platelet aggregation in diabetic patients in a dose-dependent manner, whereas 10 mmol taurine/L did not modify aggregation in healthy subjects.

Plasma and platelet taurine are reduced in subjects with insulin-dependent diabetes mellitus: effects of taurine supplementation.

Plasma and platelet taurine concentrations were assayed in 39 patients with insulin-dependent diabetes mellitus (IDDM) and in 34 control subjects matched for age, sex, and both total and protein-derived daily energy intake. Platelet aggregation induced by arachidonic acid in vitro at baseline and after oral taurine supplementation (1.5 g/d) for 90 d was also studied. Plasma and platelet taurine concentrations (mean +/- SEM) were lower in diabetic patients (65.6 +/- 3.1 mumol/L, or 0.66 +/- 0.07 mol/g protein) than in control subjects (93.3 +/- 6.3 mumol/L, or 0.99 +/- 0.16 mol/g protein, P < 0.01). After oral supplementation, both plasma and platelet taurine concentrations increased significantly in the diabetic patients, reaching the mean values of healthy control subjects. The effective dose (mean +/- SEM) of arachidonic acid required for platelets to aggregate was significantly lower in diabetic patients than in control subjects (0.44 +/- 0.07 mmol compared with 0.77 +/- 0.02 mmol, P < 0.001, whereas after taurine supplementation it equaled the mean value for healthy control subjects (0.72 +/- 0.04 mmol). In in vitro experiments, taurine reduced platelet aggregation in diabetic patients in a dose-dependent manner, whereas 10 mmol taurine/L did not modify aggregation in healthy subjects.

Effect of taurine supplementation on fat and energy absorption in cystic fibrosis.

In 10 children with cystic fibrosis and persisting steatorrhoea, supplementation with taurine (30-40 mg/kg/day) was given for two months as an adjunct to the usual pancreatic enzyme treatment. A three day fat and energy balance was performed in patients with cystic fibrosis, before and after the supplementation, and in seven healthy controls who did not receive taurine. Faecal fat was measured by a gravimetric method and stool energy was determined using a bomb calorimeter. Patients with cystic fibrosis, before and after taurine, and healthy controls received the same fat and energy intake (calculated by a dietitian). In patients with cystic fibrosis taurine did not produce any improvement of steatorrhoea (mean (SD) faecal fat 8.7 (3.3) v 11.2 (7.0) g/day, respectively before and after the supplementation), of faecal energy loss (0.978 (0.468) v 1.133 (0.539) MJ/day), of faecal fat expressed as percent of fat intake (13.4 (5.6) v 15.1 (9.8)%), and of faecal energy expressed as percent of energy intake (9.9 (3.6) v 11.2 (5.7)%). Healthy controls had significant lower fat (3.5 (2.3) g/day) and energy 0.576 (0.355) MJ/day faecal losses. In conclusion, taurine failed to decrease significantly fat and energy losses. Our study does not support the use of taurine supplementation in the nutritional management of cystic fibrosis.

High dietary taurine and feline reproduction.

Taurine is now well established as an essential nutrient for cats and may also be a conditionally essential nutrient for some other species, especially during development (Sturman, 1988). There is now a large body of literature dealing with the effects of taurine deficiency (Hayes, 1988; Sturman, 1988; Hayes and Trautwein, 1989; Sturman, 1990). Little attention has been paid to potential effects of taurine supplementation, however. In humans and cynamolgus monkeys which conjugate bile acids with taurine and glycine, the proportion of bile acids conjugated with taurine increases as the amount of taurine in the diet is increased (Sjovall, 1960; Haslewood, 1967; Hofmann and Small, 1967; Schersten, 1971; Sturman et al., 1975; Hayes et al., 1980). Such changes influence absorption from the gut, and beneficial effects of dietary taurine supplementation have been reported in chronic and acute hepatitis (Matsuyama et al., 1983; Nakashima et al., 1983), drug-induced liver disease (Attili et al., 1984), cirrhosis (Kroll and Lund, 1966), myotonia (Durelli et al., 1983), cystic fibrosis (Darling et al., 1985; Belli et al., 1987; Colombo et al., 1988; Thompson, 1988) and epilepsy (Barbeau and Donaldson, 1973; Barbeau and Donaldson, 1974; Bergamini et al., 1974; Fukuyama and Ochiai, 1982) although not in retinitis pigmentosa (Reccia et al., 1980). In addition, taurine has been added to commercial infant formulas and pediatric parenteral solutions in recent years because of mounting evidence of subtle abnormalities in visual function resulting from its absence (Sturman, 1986). A recent study reported adverse effects in the guinea pig comprising of fatty changes in the liver accompanied by changes in the lipid content after 14 days of oral administration of taurine (Cantafora et al., 1986).

The effect of taurine supplementation on the ototoxicity of neomycin in guinea pigs

Experiments have been performed to examine the effects of taurine supplementation on the ototoxicity of neomycin. It was found that concurrent administration of taurine and neomycin produced a greater degree of ototoxicity, as evidenced by increases in hearing thresholds, than with neomycin alone. The results are discussed in light of a recently proposed mechanism of aminoglycoside ototoxicity.

Taurine Improves the Absorption of a Fat Meal in Patients With Cystic Fibrosis

The effect of taurine supplementation on the absorption of a fat meal was evaluated in patients with cystic fibrosis. In a cross-over design study, five patients with cystic fibrosis (12.1 +/- 2.6 years of age) and three control subjects received either placebo or taurine (30 mg/kg/d) for two 1-week periods, a month apart, followed by a fat meal test. Blood samples were drawn 0, 1, 2, 3, 5, 8 hours after the meal. Four patients with cystic fibrosis and severe steatorrhea despite appropriate enzyme therapy showed a significant (P less than .05) improvement in the absorption of triglycerides, total fatty acids, and linoleic acid while receiving taurine supplements. Three control subjects and one child with cystic fibrosis and mild steatorrhea receiving enzyme therapy did not experience such an effect. The difference in triglyceride absorption, when calculated as the area under the curve, receiving and not receiving taurine was significantly (P less than .05) correlated with the degree of steatorrhea. Furthermore, in contrast to control subjects, the fatty acid composition of chylomicrons in these four study patients showed important discrepancies with that of the fat meal and was corrected, in part, by taurine supplementation. These results suggest that taurine supplementation could be a useful adjunct in the management of patients with cystic fibrosis with ongoing fat malabsorption and essential fatty acid deficiency.

Taurine supplementation, fat absorption, and growth in cystic fibrosis

The effect of taurine supplementation (30 to 40 mg/kg/24 hr) on fat absorption and related measurements was examined in 21 preadolescent children with cystic fibrosis (CF) using a 12-month double-blind crossover technique. The mean coefficient of fat absorption was unchanged by taurine both in the unselected study group (without taurine, mean +/- SD 84.0% +/- 11.9%; with taurine, 84.4% +/- 11.8%, n = 20) and in a subgroup of seven children with moderately severe fat malabsorption (without taurine, 75.6% +/- 15.6%; with taurine, 74.8% +/- 14.6%). The mean fecal split fat/total fat ratio, which generally reflects bile acid-related fat malabsorption, was also unchanged. Linoleic and arachidonic acid deficiencies noted in plasma before supplementation showed no significant improvement with taurine supplementation. Likewise, plasma/serum vitamin A, E, and D levels were unchanged. Standard scores for height and weight were not affected significantly. This study does not support the use of taurine supplementation in the nutritional management of CF.

Effect of taurine supplementation on bile acids composition in infants on total parenteral nutrition (TPN) : E. Marinier, D. Feldman, P. Aymard, J.P. Cezard, J. Navarro. Hôpital Bretonneau et Trousseau, Paris. France

Effect of taurine supplementation on bile acids composition in infants on total parenteral nutrition (TPN) : E. Marinier, D. Feldman, P. Aymard, J.P. Cezard, J. Navarro. Hôpital Bretonneau et Trousseau, Paris. France

Effect of Taurine Supplementation on Hepatic Function During Short‐Term Parenteral Nutrition in the Premature Infant

To evaluate the potential role of taurine deficiency in the pathogenesis of parenteral nutrition‐induced cholestasis, 20 premature (&lt;34 weeks AGA) infants were randomized to receive parenteral nutrition with and without taurine (10.8 mg/kg/day) during the first 10 days of life. Birth weight, gestational age, and protein and caloric intake were similar in both groups. Plasma taurine levels and hepatic function were assessed before the study began (3 ± 1 days of age), at 5 ± 1 days of age, and at 9 ± 1 days of age. Although plasma taurine levels were significantly greater at 5 ± 1 and 9 ± 1 days of age (p = 0.009) in the group receiving supplementation, no differential effect on hepatocellular function could be detected during this short period of time. A decrease in plasma ammonia (p = 0.001), alanine aminotransferase (ALT) (p = 0.036), γ‐glutamyltranspeptidase (GGTP) (p = 0.05), 5‐nucleotidase (5'N) (p = 0.001), and bile salt concentrations was noted in both groups, indicating the rapid maturation of hepatic function even in the presence of parenteral nutrition during the first 10 days of life.