Taurine: an essential nutrient for the cat

Cats fed a purified diet containing purified casein as the source of protein develop retinal degeneration due to the lack of taurine in the diet. To test whether cats can synthesize this sulfur amino acid from sulfate or cystine, radioisotopes of these substances were injected into taurine-depleted and control cats. Sulfate did not serve as a precursor for taurine synthesis, whereas cystine underwent only a moderate conversion to taurine. This is in keeping with the low level of cysteinesulfinic acid (CSA) decarboxylase activity in cat liver. There was no difference between the activity of CSA decarboxylase in tissues from control cats and that in tissues from taurine-depleted cats. The pattern of tissue accumulation of [35S]taurine and from [35S]cystine also indicated that tissues from taurine-depleted cats do not synthesize [35S]taurine more rapidly than tissues from control cats. The data did not indicate a difference in taurine uptake by tissues of control and deficient cats, but progressive accumulation in deficient cats suggested that the turnover rate of taurine is decreased by the deficiency. Since supplementation of the purified diet with cysteine has been found previously to be inadequate to prevent progressive taurine depletion of the retina and its subsequent degeneration and since conversion of sulfur compounds to taurine in vivo is inadequate, taurine can be considered an essential nutrient for the cat.     

Dietary taurine content changes liver lipids in cats.

Adult female cats were fed a completely defined purified diet (taurine-free) alone or containing 0.05% taurine (the normal dietary requirement) or 1% taurine (20-fold the normal dietary requirement) for greater than 2 y. The relative composition of conjugated biliary bile acids was not different among the three groups and virtually all bile acids were conjugated with taurine. The taurine concentration in liver varied dramatically with the amount of taurine in the diet. Total liver lipid content decreased with increasing dietary taurine. Individual lipid components also varied, especially free fatty acids (which decreased with increasing dietary taurine) and triglycerides (which increased with increasing dietary taurine), indicating that taurine has a metabolic effect on lipid metabolism. Taurine deficiency also caused significant changes in the fatty acid distribution of sphingomyelin. In particular, a decrease of lignoceric acid and an increase of nervonic acid were observed. The present data suggest that hepatocellular levels of taurine can modulate the mobilization of liver lipid stores and the utilization by the liver of circulating free fatty acids. These effects are probably mediated by factors affecting membrane fluidity, such as the ratio of cholesterol to phospholipids, the degree of unsaturation of phospholipids and the changes in sphingomyelin fatty acid composition.     

Feline maternal taurine deficiency: effect on mother and offspring

Adult female cats were fed a defined purified diet (taurine-free) either alone or supplemented with 0.05% taurine for at least 6 mo prior to breeding. The reproductive performance by the taurine-depleted females was poor, whereas those receiving dietary taurine had normal pregnancies and deliveries. The taurine-depleted females suffered from severe retinal degeneration, including a large loss of photoreceptor outer segments, and degeneration of the tapetum lucidum, and greatly reduced concentrations of taurine in their body tissues and fluids. Surviving offspring from the taurine-depleted mothers exhibited a number of neurological abnormalities and substantially reduced concentrations of taurine in the body tissues and fluids. Except for greater concentrations of cystathionine in neural tissues, other free amino acids in tissues were unaffected. The specific activities of a number of enzymes involved in the biosynthesis of taurine were unchanged in liver and brain. The composition of maternal milk, total protein, protein amino acids and free amino acids was unchanged except for taurine content, suggesting that the abnormalities in the offspring resulted from the diminished dietary taurine.     

Effect of processing on fate of dietary [14C]taurine in cats

The objective of this study was to determine the fate of a pulse-labeled oral dose of uniformly labeled [14C]taurine in cats fed four separate diets. The diets were a heat-processed commercial diet, the same diet frozen-preserved and two purified diets containing 0 or 1325 mg taurine/kg. The commercial formulations contained 1070 mg taurine/kg dry matter (by analysis). The excretion of 14C in CO2, urine and feces was monitored. Significant quantities of 14CO2 were produced, with greater amounts excreted by cats fed the heat-processed commercial diet (9.4% of initial dose) than by those fed the frozen-preserved diet (0.09%), indicating extensive taurine degradation by the intestinal microflora. Purified diet groups were intermediate between the two commercial diet groups. Carbon-14 excreted in urine peaked at 24 h and was highest for cats fed the frozen-preserved commercial diet or 1325 mg taurine/kg purified diet. Carbon-14 excreted in feces was highest for cats fed the two commercial diet formulations, with peak amounts at 48-72 h. Because the frozen-preserved commercial diet had previously been shown to maintain plasma taurine concentration, whereas the heat-processed diet did not, these results indicate that processing affects the digestive and/or absorptive process in a manner that increases the catabolism of taurine by gastrointestinal microorganisms.     

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.     

High dietary protein and taurine increase cysteine desulfhydration in kittens

The objective of this study was to determine the effect of dietary protein and taurine on cysteine desulfhydration in various kitten tissues. Cysteine desulfhydration was assessed in liver, kidney, skeletal muscle, heart, spleen, brain and jejunum of kittens fed one of the following diets for 5 wk: 20% protein, 0% taurine diet (LP0T); 20% protein, 0.15% taurine diet (LPNT); 60% protein, 0% taurine diet (HP0T); and 60% protein, 0.15% taurine diet (HPNT). Cats fed LP0T and HP0T had been fed a taurine-free diet for 10 wk before the 5-wk experiment. The activity of cysteine desulfhydration was determined by measuring the production of H(2)(35)S from (35)S-cysteine in the presence and absence of alpha-ketoglutarate (alphaKG) in the incubation medium. Liver and kidney had the highest total activities among the tissues tested (P < 0.01). Total hepatic desulfhydration activities [micromol H(2)S/(min. kg body wt)] in cats fed LP0T, LPNT, HP0T and HPNT were (mean +/- SEM) 117 +/- 6, 135 +/- 10, 137 +/- 10 and 190 +/- 9, respectively. Dietary taurine had a significant effect on activity when expressed per gram liver (P < 0.01), per gram protein (P < 0.05) and per kilogram body weight (P < 0.001). Dietary protein had a significant effect (P < 0.001) only when activity was expressed relative to body weight because of the significant effect of protein on relative liver weight. The direct pathway via cysteine desulfhydrase appears to be the major route of cysteine desulfhydration in kitten liver because the values obtained in the absence of alphaKG were 81-88% of those obtained in the presence of alphaKG.     

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 protein source (soybean vs. casein) and taurine status affect kinetics of the enterohepatic circulation of taurocholic acid in cats.

The effect of dietary protein source (soybean vs. casein) and taurine status on kinetics of [24-14C] and [taurine-2-3H]taurocholic acid was determined by isotope dilution in 10 adult male cats (six taurine-replete and four taurine-depleted). Taurine-replete cats were fed 1500 mg taurine/kg purified diets containing either 435 g/kg casein (1500 Cas) or soybean protein (1500 Soy) in a crossover design. Taurine-depleted cats were fed the soybean protein diet with no taurine (0 Soy). Specific activity of [14C]- and [3H]taurocholic acid in bile was determined for 6 d following a pulse dose of dual-labeled taurocholic acid. Taurocholic acid pool size was significantly greater in cats when fed the 1500 Soy diet than when fed the 1500 Cas or than in cats fed the 0 Soy diet. Total entry rate, irreversible loss rate and recycling rate of [taurine-2-3H]taurocholic acid and the irreversible loss rate of [24-14C]taurocholic acid tended to be greater in cats when fed the 1500 Soy than the 1500 Cas diet. Irreversible loss rates of taurocholic acid in taurine-replete cats fed the 1500 Soy diet were significantly greater than in taurine-depleted cats, 356 vs. 120 mumol/d [24-14C]taurocholic acid and 445 vs. 56 mumol/d [taurine-2-3H]taurocholic acid. The fraction of taurocholic acid was greater, and the fraction of taurochenodeoxycholic and taurodeoxycholic acids lower in cats when fed the 1500 Soy than when fed the 1500 Cas diet. Taurine-depleted cats had less taurocholic, taurochenodeoxycholic, and taurodeoxycholic acids and greater glycocholic and cholic acids than taurine-replete cats fed the 1500 Soy diet. This study demonstrates that both dietary protein source and taurine status affect taurocholic acid kinetics and bile acid composition in cats.     

Taurine balance is different in cats fed purified and commercial diets.

Ileal fluxes, urinary losses and taurine balance were determined in six taurine-replete and four taurine-depleted cats. Digesta samples collected at the terminal ileum were used to assess ileal flux of taurine. Four diets were tested: a commercial diet in two forms (heat-processed and frozen) and two purified diets containing either 1225 or 0 mg taurine/kg diet. Five-day balance trials were performed on d 3-7 with measurement of food intake and taurine in urine and ileal digesta. Substantially greater quantities of total taurine (free + bound) were found in ileal digesta from cats fed the heat-processed rather than the frozen preserved diet (205 vs. 101% of the average daily taurine intake, respectively), with calculated taurine balances of -609 vs. -212 mumol/d, respectively. The quantity of taurine in ileal digesta from taurine-replete cats fed the 1225 or 0 mg taurine/kg purified diets was not significantly different, indicating that taurine found at the terminal ileum is mostly of endogenous origin. Taurine-depleted cats had significantly lower amounts of taurine in ileal digesta, with a taurine balance of -77 mumol/d. These results demonstrate that a heat-processed diet causes substantially greater losses of taurine from the intestine than does a frozen diet. This phenomenon may explain the inability of some heat-processed diets to maintain normal plasma taurine concentrations in cats.     

High dietary taurine effects on feline tissue taurine concentrations and reproductive performance.

The reproductive performance and outcome of kittens was determined for female cats fed 0.05, 0.2 or 1% taurine. No adverse effects of high taurine diets were noted in the adults or offspring, and the reproductive performance was slightly better than that of females fed the normal (0.05% taurine) diet. Body weight at birth and brain weight at weaning were significantly greater in the very high taurine group than in the normal taurine group, although the greatest growth rate was achieved by the normal taurine group. The concentration of taurine in milk of lactating females was substantially higher in cats fed the higher taurine diets. Brain of adult cats was resistant to increases in brain taurine concentrations, as was brain of newborn cats. However, brain of juvenile cats responded to higher dietary taurine intake with increased taurine concentrations. These results indicate that the higher taurine content in cat foods recently introduced for prevention of feline dilated cardiomyopathy should have no adverse effects over a prolonged period on health and reproduction of cats.     

Effect of diet on plasma taurine in the cat

Near adult cats were deprived of dietary taurine until the plasma levels were consistently below 10 microM. The source of dietary lipid (animal versus vegetable), source of protein (soy versus casein versus tuna) and level (17%, 34%, 70%) and the sulfur amino acid content of the diet were then independently varied to determine their respective effects on plasma taurine. Plasma taurine was not influenced by the source of dietary fat but was sensitive to the sulfur amino acid content of the diet independent of total protein when methionine plus cystine was below 1.55% of the diet. Therefore, it is suggested that below 1.55% total sulfur amino acids the taurine requirements of the cat may be a function of the sulfur amino acid content of the diet. No retinal lesions in the area centralis occurred.     

TAURINE INVOLVEMENT IN RETINAL AND HEART MUSCLE FUNCTION

Retinal photoreceptor cells degenerate in cats fed a diet low in sulfur amino acids and sulfate. The formation of taurine from sulfate appears to be an important pathway in heart and liver in many species, especially in the cat. Elevated heart taurine levels have been found in patients dying from congestive heart disease, but not in skeletal muscle of hypertensive rats.     

Taurine supplementation in infants receiving long-term total parenteral nutrition.

Twenty-one children and 23 adults receiving long-term total parenteral nutrition (TPN) for 27 +/? 23 (SD) months were investigated to determine if they were taurine-deficient because the TPN solutions were taurine-free. The fasting plasma taurine level was reduced in the children to 26 + 13 mumol/liter vs the control 57 +/? 16 mumol/liter (P greater than 0.001). The plasma taurine level was significantly reduced in those adults who absorbed less than 25% of their nutritional needs from their diet. Electroretinograms were abnormal in each of eight children who were examined; isolated cone and rod implicit times were both significantly delayed. Electroretinograms were not abnormal in those adults with low plasma taurine levels. Taurine was added to the TPN solutions of four children, and the plasma taurine level became normal in each of them. Electroretinograms of three of these children became normal. One year after discontinuing intervenous taurine supplementation, the plasma taurine level became abnormal in two of three children. These observations indicate that children, and possibly adults, receiving long-term TPN have a nutritional requirement for taurine.     

Taurine supplementation in infants receiving long-term total parenteral nutrition

Twenty-one children and 23 adults receiving long-term total parenteral nutrition (TPN) for 27 +/- 23 (SD) months were investigated to determine if they were taurine-deficient because the TPN solutions were taurine-free. The fasting plasma taurine level was reduced in the children to 26 + 13 mumol/liter vs the control 57 +/- 16 mumol/liter (P greater than 0.001). The plasma taurine level was significantly reduced in those adults who absorbed less than 25% of their nutritional needs from their diet. Electroretinograms were abnormal in each of eight children who were examined; isolated cone and rod implicit times were both significantly delayed. Electroretinograms were not abnormal in those adults with low plasma taurine levels. Taurine was added to the TPN solutions of four children, and the plasma taurine level became normal in each of them. Electroretinograms of three of these children became normal. One year after discontinuing intervenous taurine supplementation, the plasma taurine level became abnormal in two of three children. These observations indicate that children, and possibly adults, receiving long-term TPN have a nutritional requirement for taurine.     

Taurine and serine supplementation modulates the metabolic response to tumor necrosis factor alpha in rats fed a low protein diet.

Plasma taurine and serine decrease following trauma and in severe inflammatory disease. These changes may signify an increase in requirements for sulfur amino acids. We previously demonstrated that cysteine supplementation can restore the impaired ability of rats fed an 8% casein diet to increase hepatic zinc, glutathione (GSH) and protein concentrations in response to tumor necrosis factor alpha (TNF alpha). Here we examined whether serine or taurine produces a similar effect, because serine provides the carbon skeleton of cysteine and taurine is its major metabolite. After 7 d of receiving either a 20% casein diet supplemented with cysteine or an 8% casein diet supplemented with alanine, serine or taurine, rats received an intraperitoneal injection of human TNF alpha. Tumor necrosis factor caused no change in hepatic GSH but resulted in a lower GSH concentration in lung in rats fed the alanine-supplemented diet. Neither taurine nor serine increased liver GSH relative to that in rats fed alanine, but the depression in lung due to TNF injection was lessened. The absolute increase in ceruloplasmin in response to TNF was enhanced in rats fed the alanine-supplemented diet relative to those fed the 20% casein diet. Serine normalized this response. This observation--the effects of taurine and serine on lung GSH and a significant negative correlation between ceruloplasmin and liver and lung GSH concentration in rats fed TNF--suggests that supplemental serine and taurine may improve antioxidant defenses when dietary supplies of cysteine are low but do not influence cysteine availability for a normal response to TNF.     

牛磺酸对单眼剥夺大鼠视觉中枢nNOS表达的影响

目的:观察牛磺酸喂养对单眼剥夺大鼠视觉中枢神经型一氧化氮合酶(nNOS)阳性神经元表达的影响,探讨牛磺酸是否具有拮抗单眼剥夺所致的弱视效应。方法:新生健康雄性大鼠随机分成正常对照组、单眼剥夺组和单眼剥夺牛磺酸喂养组。免疫细胞化学染色观察剥夺眼对侧视觉中枢nNOS阳性神经元表达的变化。结果:①nNOS阳性神经元散在分布于视皮质V1区Ⅱ～Ⅵ层和外膝体背核,形态学均表现为中间神经元。②单眼剥夺2周后,剥夺对侧视觉中枢阳性神经元表达减弱,和单眼剥夺组比较,牛磺酸喂养组阳性神经元表达增强,但仍达不到正常。结论:在中枢神经系统发育中起重要作用的牛磺酸经由一氧化氮(NO)介导可以拮抗大鼠单眼剥夺性弱视,因此作为弱视治疗的可行药物有待深入研究。     

Hepatic cysteine dioxygenase activity and sulfur amino acid metabolism in rats: possible indicators in the evaluation of protein quality

Experiments were carried out to examine the possibility that the sulfur amino acid metabolism of rats may be an indicator of the nutritional value of dietary protein. Rats were fed diets containing 8, 16 or 24% of gluten, soy protein or casein for 3 wk. Hepatic cysteine dioxygenase activity, hepatic concentration of glutathione, cysteine and taurine and urinary taurine were examined. In addition, the sulfur amino acid metabolism of rats fed these diets fortified with the appropriate first limiting amino acid for 7 d was also examined. High urinary taurine excretion was observed in the three gluten groups, whereas very low urinary taurine excretion was observed with up to 24% soy protein or up to 16% casein. The hepatic hepatic cysteine dioxygenase activities of the gluten diet groups were higher than those of corresponding soy protein or casein diet groups, except that of rats fed the 24% casein diet. The hepatic concentrations of both glutathione and cysteine in gluten diet groups were also higher than those of corresponding soy protein or casein diet groups, except 24% soy protein and 16 and 24% casein diet groups. In rats fed the casein or soy protein diets urinary taurine excretion and hepatic cysteine dioxygenase activity increased with increasing methionine supplementation, the first limiting amino acid. Conversely, in rats fed the gluten diet both urinary taurine excretion and hepatic cysteine dioxygenase activity decreased with increasing lysine supplementation, the first limiting amino acid. These findings suggest that urinary taurine excretion and hepatic cysteine dioxygenase activity may be useful as sensitive indicators of the nutritional value of dietary protein.     

The effect of dietary protein on nitrogen and sulfur metabolism in portacaval-shunted rats

The effect of varying the amount of protein in the diet on postoperative recovery, plasma ammonia, urinary orotic acid and metabolism of sulfur-containing amino acids was examined in rats with portacaval shunts (PCS). Food intake and weight gain were lower in both PCS and control rats fed a low (6%) casein diet unsupplemented with methionine compared with rats fed an adequate (18%) casein diet. PCS rats fed 60% casein ate slightly less and took longer to recover their preoperative body weight compared to 60% controls. Shunted rats were consistently hyperammonemic and orotic aciduric compared to controls. Increasing protein in the diet elevated plasma ammonia and urinary orotic acid in all rats to levels above those of the rats fed 18% casein, but the effect was greater in rats with PCS. After i.p. injection of L-[35S]methionine or L-[35S]cysteine, urinary 35S and [35S]sulfate excretion increased and [35S]taurine and total taurine excretion decreased in all rats fed 60% casein. These changes are consistent with our observation that hepatic activities of cysteine dioxygenase and cysteine sulfinate:alpha-ketoglutarate aminotransferase increased and that of cysteine sulfinate decarboxylase decreased in rats fed the high protein diet. The effect of dietary treatment on both urinary taurine excretion and decarboxylase activity was greater in PCS rats than in controls. Although PCS rats fed a high protein diet may have a decreased taurine-synthesizing capability compared to controls, their ability to oxidize a methionine or cysteine load to sulfate is not compromised by feeding either an 18 or 60% casein diet.     

Studies on renal adaptation to altered dietary amino acid intake: tissue taurine responses in nursing and adult rats

This study examines the effect of a low sulfur amino acid diet (LTD) and a high taurine diet (HTD), compared with a normal diet, on the plasma, urine, muscle, brain and renal cortex levels of taurine in immature and adult rats. Milk taurine from lactating dams reflected the taurine content of the diet, being low in LTD-fed and high in HTD-fed animals. Nursing pups (7, 14 and 21 d old) often had plasma, urine and tissue--renal cortex, heart, skeletal muscle--levels of taurine related to dietary exposure, a situation also found in adult animals. These diets did not influence the urinary excretion of the sulfur-containing alpha-amino acids methionine and cystine but a sulfur aminoaciduria of immaturity was evident. By contrast, the content of taurine in brain was constant regardless of dietary intake of sulfur amino acids. An age-related decline in brain taurine content was found--as noted by others--but this too was influenced by diet. This dual finding of brain taurine constancy despite wide differences in sulfur amino acid intake and changes in the renal handling of taurine as influenced by diet suggest that the renal adaptive response serves to maintain the stability of brain taurine content.     

Tissue taurine content, activity of taurine synthesis enzymes and conjugated bile acid composition of taurine-deprived and taurine-supplemented rhesus monkey infants at 6 and 12 mo of age

Concentrations of taurine were measured in a number of tissues from rhesus monkeys fed a taurine-free human infant formula with or without taurine supplementation for 6 mo and 12 mo. At 6 mo, tissue taurine content was significantly greater in the monkeys supplemented with taurine, but by 12 mo, there was no longer a significant difference. Activities of enzymes involved in taurine biosynthesis did not differ between the groups at any age. There was no difference in biliary bile acid class composition between the groups, but the proportion of bile acids conjugated with taurine reflected the tissue taurine content (i.e., was significantly greater in monkeys supplemented with taurine at 6 mo). This difference also disappeared by 12 mo. These results indicate that dependence on dietary sources of taurine persists for at least the first 6 mo but declines by 12 mo. Thus, dietary taurine content is reflected in the tissue taurine content and proportion of bile acids conjugated with taurine in infant rhesus monkeys at least until 6 mo of age, but the body taurine status in animals 12 mo old or older is not an indicator of previous status.