Urinary Taurine Excretion Research Articles

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:α-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.

Renal cortex taurine content regulates renal adaptive response to altered dietary intake of sulfur amino acids.

Rats fed a reduced sulfur amino acid diet (LTD) or a high-taurine diet (HTD) demonstrate a renal adaptive response. The LTD results in hypotaurinuria and enhanced brush border membrane vesicle (BBMV) accumulation of taurine. The HTD causes hypertaurinuria and reduced BBMV uptake. This adaptation may relate to changes in plasma or renal cortex taurine concentration. Rats were fed a normal-taurine diet (NTD), LTD, or HTD for 14 d or they underwent: (a) 3% beta-alanine for the last 8 d of each diet; (b) 3 d of fasting; or (c) a combination of 3% beta-alanine added for 8 d and 3 d of fasting. Each maneuver lowered the cortex taurine concentration, but did not significantly lower plasma taurine values compared with controls. Increased BBMV taurine uptake occurred after each manipulation. Feeding 3% glycine did not alter the plasma, renal cortex, or urinary taurine concentrations, or BBMV uptake of taurine. Feeding 3% methionine raised plasma and urinary taurine excretion but renal tissue taurine was unchanged, as was initial BBMV uptake. Hence, nonsulfur-containing alpha-amino acids did not change beta-amino acid transport. The increase in BBMV uptake correlates with the decline in renal cortex and plasma taurine content. However, since 3% methionine changed plasma taurine without altering BBMV uptake, it is more likely that the change in BBMV uptake and the adaptive response expressed at the brush border surface relate to changes in renal cortex taurine concentrations. Finally, despite changes in urine and renal cortex taurine content, brain taurine values were unchanged, which suggests that this renal adaptive response maintains stable taurine concentrations where taurine serves as a neuromodulator.

Methionine metabolism after portacaval shunt in the rat.

The effect of portacaval shunt (PCS) on methionine metabolism in the rat was investigated. Male Sprague-Dawley rats were subjected to PCS and maintained on an 18% casein diet. Growth curves of operated rats were similar to controls. PCS rats excreted more urinary 35SO4 and less [35S]taurine than controls after intraperitoneal injection of 0.3 mmol/100 g [35S]methionine or [35S]cysteine. Total urinary taurine excretion was similar in PCS and control rats after a methionine or cysteine load; however, under basal conditions PCS rats had higher urinary taurine levels than controls, indicating that PCS may cause the taurine pool to be expanded. Hepatic methionine, S-adenosylmethionine, and cysteine pools were significantly decreased in PCS rats, while S-adenosylhomocysteine levels were unchanged. Relative rates of transsulfuration in PCS and control rats were studied by following the decrease in the 3H-to-35S ratio in liver protein after injection of [methyl-3H]methionine and [35S]methionine, and no difference in flux of 35S from [35S]methionine to [35S]cysteine was found. Similarly, total hepatic activities of methionine adenosyltransferase, cystathionine synthase, and cystathionine gamma-lyase were unchanged in PCS rats. These results indicate that altered methionine metabolism in PCS rats is not explained by changes in conversion of methionine to cysteine via the transsulfuration pathway.

Studies on the role of taurine in Friedreich's ataxia

New studies were undertaken to verify the previous findings of increased urinary excretion of taurine, in the basal state and after challenge with a taurine load, in Friedreich's disease. Particular attention was paid to possible causes of error such as weight, muscle mass, creatine and creatinine excretion, variability with time and appropriate control groups. Although the overall findings were confirmed, their interpretation is open to question because of all these factors of error. Many possibilities must still be further explored to account for the apparent taurine retention defect observed in many cases of Friedreich's disease.

Changes in maternal taurine levels in response to pregnancy and lactation

Taurine levels in various tissues and fluids of female rats were measured throughout pregnancy and lactation. The taurine concentration of liver markedly increased at days 19 and 21 of pregnancy to 188% of levels for nonpregnant, nonlactating control rats and then fell rapidly after delivery to reach only 30% of the control level by 3 days post-partum. Muscle and heart taurine concentrations were significantly negatively correlated with liver taurine levels. Brain taurine levels were low at days 14, 19 and 21 of pregnancy and day 14 of lactation. Urinary excretion of taurine decreased to 32% of control levels at day 21 of pregnancy and was negatively correlated with the hepatic taurine concentration over the course of pregnancy and lactation. The ratio of glycine- to taurine-conjugated bile acids was strongly negatively correlated with the hepatic taurine concentration. The milk taurine level was positively correlated with hepatic taurine concentration during lactation. The hepatic taurine pool appears to increase just before parturition and to rapidly decrease during the first few days of lactation when high levels of taurine are secreted in the milk. Our data suggests that the accumulation of taurine in the liver may be related to both a decreased renal clearance of taurine and a shifting of tauring from other tissues to the liver and that this enlarged pool of hepatic taurine may serve as a source of taurine for secretion in the early milk.

Taurine Concentration in the Perinatal Period

AbstractA study was made on the concentration of taurine in the cord blood, maternal serum, breast milk, urinary excretion and plasme of the same mothers and newborns. The results showed that the taurine content in maternal serum taken within 24 ours of delivery was 117.3 n mol/ml and that of cord blood was 303.5 n mol/ml giving a ratio of 1:2.6. The taurine in breast milk on day 1 and 2 was low but there was a daily increase and on teh 7th day its average became 381.8 n mol/ml.The urinary excretion of taurine in teh newborn was 6,222 n mol/ml before the initial feeding on the 1st day. A gradual decrease was noted and on the 5th day it was 1/15 of tat of the first day.Plasma taurine of the newborn was 186.7 n mol/ml on the first day decreasing to 85.2 n mol/ml on the 5th day.There was a lesser tendency for taurine in the plasma and urine to decrease in the breast fed as compared with those on formulas.

Role of taurine in feeding the low-birth-weightinfant

Plasma and urinary taurine concentrations, growth, nitrogen balance, duodenal bile salt concentration and pattern, fecal bile acid excretion, and intestinal fat absorption were determined in appropriate for gestational age low-birth-weight infants fed either a whey-predominant cow milk formula or the same formula supplemented with taurine (45 mumol/kg/day). Mean plasma taurine concentration in the two groups did not differ. Mean urinary taurine concentration in the control and supplemented groups over the entire study period were 2.67 +/- 0.69 and 12.41 +/- 5.20 mumol/dl, respectively (P less than 0.05). Urinary taurine concentration in the supplemented infants, however, decreased significantly during the study period. Neither growth nor nitrogen retention differed between the two groups. Mean duodenal concentrations of taurine as well as glycine conjugates of both cholate and chenodeoxycholate were higher in supplemented infants. Total duodenal bile salt concentration correlated positively with taurine status as reflected by urinary taurine excretion (r = 0.71); this correlation plus the lower duodenal cholesterol concentration in supplemented infants suggests that conversion of cholesterol to bile acids was greater in supplemented infants. Mean intestinal fat absorption in control and supplemented infants, however, did not differ.

Taurine transport in brush border membrane vesicles isolated from hyper- and normotaurinuric mouse kidney.

The mouse strain C57BL is characterized by a high urinary fractional excretion of taurine. Hypertaurinuric [tau(-)] C57BL mice and three normal taurine 'excretors' [tau(+)]-Swiss, A/J, and C3H-were compared. Clearance experiments showed that fractional excretion of taurine was 4-8 times higher in C57BL relative to the other strains. Transport studies performed in brush border membrane vesicles, isolated from C57BL and C3H mouse renal cortex, showed that D-glucose uptake was similar in both strains while the taurine uptake appeared to be faster in tau(+) than in tau(-) mice. This difference was observed only in the presence of an inwardly directed NaCl gradient. The comparison of kinetic parameters showed a significant difference of apparent Km values: 90.8 +/- 11.4 microM in tau(+) mice vs. 129.5 +/- 17.1 microM in tau(-) mice. Jmax were not significantly different in both strains. These observations suggest a lower affinity of the taurine brush border membrane carrier in the hypertaurinuric strain as compared to the normotaurinuric mice. It is concluded that, in addition to a possible alteration of peritubular taurine efflux described by Rozen et al. (1983), a defect of taurine transport at the luminal membrane cannot be excluded and could account for the hypertaurinuria of the C57BL mice.

Urinary excretion of taurine in epilepsy.

The level of urinary taurine and 17-hydroxycorticosteroids were estimated in 19 cases of epilepsy. These levels were then compared with those of normal healthy subjects. The urinary taurine levels were significantly higher in epilepsy and have diagnostic as well as prognostic significance.

Renal adaptation to alteration in dietary amino acid intake.

The nonessential beta-amino acid taurine, which is inert in renal tissue, was used to study the renal adaptation to dietary taurine change. Three isoproteinic diets were employed: HTD--high in taurine, NTD--normal taurine, and LTD--deficient in the taurine precursors cysteine and methionine. When compared with NTD, HTD resulted in an increase in the urinary excretion and fractional excretion of taurine, whereas LTD led to a decrease in urinary excretion and fractional excretion of taurine. In vitro studies demonstrated an increase in the Vmax of the high-affinity, low-capacity uptake system with no change in "apparent" Km following LTD. Complete adaptation developed within days after the diet was changed (NTD to HTD = 3 days; NTD to LTD = 3-6 days). These studies demonstrate that the renal response to altered dietary amino acid can be evaluated and that adaptation occurs for the beta-amino acid taurine. The renal response serves to conserve taurine during periods of deprivation and to dispose of taurine during periods of excess. The renal adaptation to restricted taurine intake seems to occur through an increase in transport sites (increased Vmax) or change in flux at the transport sites, with no change in transport affinity (unaltered apparent Km).

Decrease of urinary taurine in essential hypertension.

In order to evaluate how taurine relates to the pathogenesis of essential hypertension, the taurine content of plasma, whole blood and urine was measured in 18 normals and in 79 hypertensive patients. The patients included 32 untreated cases of essential hypertension, 32 treated cases and 15 cases with labile hypertension. There were no statistically significant differences between normals and essential hypertensives in either plasma or whole blood taurine content. However, in comparison to urinary taurine excretion in normals, 1594.0 +/- 143.7 mumol/day (mean +/- SE), that for untreated essential hypertensives, 708.1 +/- 57.1 mumol/day (p less than 0.001), and for treated essential hypertensives, 953.6 +/- 94.3 mumol/day (p less than 0.001), were significantly lower. Those with labile hypertension showed almost the same value, 1478.3 +/- 134.3 mumol/day, as normals. Taurine clearance and the taurine/creatinine ratio were also markedly decreased in essential hypertensives without treatment. For all subjects, taurine clearance had a positive correlation (r = 0.327, p less than 0.01) with creatinine clearance, but there were significant negative correlations between systolic blood pressure and daily urinary taurine excretion (r = -0.472, p less than 0.01) and between diastolic blood pressure and daily urinary taurine excretion (r = -0.382, p less than 0.01). There were also significant positive correlations between daily urinary taurine excretion and serum high-density lipoprotein cholesterol (r = 0.559, p less than 0.01) and between the former and cardiac index (r = 0.547, p less than 0.01). These results suggest that a deficiency of taurine plays an important role not only in elevating blood pressure in essential hypertension but also in atherogenesis as well.

Fasting reverses the renal adaptation to altered dietary sulfur amino acid intake.

AbstractWe have previously shown that there is renal adaptation to alterations in dietary sulfur amino acid intake. While ingesting a low-methionine, low-taurine diet, urinary and plasma taurine concentrations fall, and the accumulation of taurine by collagenaseisolated tubules is greatly enhanced. On a taurine and methionine-supplemented diet (3%, w/w), urinary and plasma taurine values are increased, and accumulation by tubules is diminished. This study was planned to evaluate the effect of fasting on the adaptation to dietary intake change. Rats were given a high-taurine diet (HTD), low-taurine diet (LTD), or a normal diet (NTD) from age 56 to 70 days of life. Half of the rats in each dietary group were fasted for 72 hr and they lost 13 ± 1% of body weight. Plasma taurine values fell in all three fasted groups, and urinary taurine excretion rose in LTD and fell in HTD-fasted animals. Renal cortex taurine fell in all fasted groups, indicative of taurine release. The in vivo tissue distribution ratio rem...

A possible genetic pattern of taurine urinary excretion in Friedreich's Ataxia.

The taurine urinary excretion pattern, before and after an oral load of 250 mg taurine, was studied in normal control subjects and in patients with typical Friedreich's ataxia. It was demonstrated that in both situations the ataxic patients fell within the sub-types of "intermediate" and "high taurine excretors" while non were "low taurine excretors". It was also demonstrated that the excretion of taurine after a load in the obligate heterozygotes parents of the ataxic patients was intermediate between normal controls and patients. It is postulated that patients with Friedreich's Ataxia lack normal regulation of the high affinity-low capacity uptake system for taurine (the TH system) in the brush border of kidney tubules. The low affinity-high capacity uptake system in the same membranes (the TL system) appears to be normal in Friedreich's patients. The normal allele could be called THN and the variant THF and this trait would be inherited in an autosomal recessive fashion if it is linked to the Friedreich phenotype. Whether this finding is or is not the basic genetic defect in Friedreich's Ataxia will require more studies to clarify, but it is of interest to note that a similar pattern appears to be present in the fibroblasts of these patients.

Dietary adaptation of taurine transport by rat renal epithelium

Taurine, a β-amino acid, was used as a marker to study the effect of dietary amino acid manipulation on β-amino acid transport by rat renal epithelium. Adult (57–58 day old) rats were maintained on high-taurine; normal-taurine, normal-methionine; and low taurine, low-methionine diets. Urinary excretion and fractional excretion of taurine rose with the high-taurine diet and diminished with the low-taurine diet. Uptake of taurine was then studied using suspensions of isolated cortical tubule segments. When compared to normals, uptake was lower in the high-taurine group and greater in animals on the low-taurine diet. Evaluation of uptake kinetics shows an increase in maximum velocity (Vmax) with low-taurine diet, with no change in “apparent” Km. This suggests that the adaptation to dietary amino acid manipulation occurs through an alteration in the number of uptake sites, with no change in the affinity of the uptake system for the amino acid.

Comparative metabolism and taurine-depleting effects of guanidinoethanesulfonate in cats, mice, and guinea pigs

Guanidinoethanesulfonate (GES) is a competitive inhibitor of taurine transport. The ability of GES to deplete taurine content has been compared in three species representing omnivores, carnivores, and herbivores. Rats and mice given drinking water containing 1% GES showed large decreases in taurine concentration in all examined organs within a few days. These species do not metabolize GES. The substance was without effect on guinea pigs, a species that does not depend on diet for taurine, even after 20 days of treatment. However, guinea pigs metabolize a fraction of the GES administered to taurine. Cats responded to GES by increasing their urinary excretion of taurine 10-fold, while simultaneously maintaining normal concentrations in body organs. [1,2- 3H]GES given orally to cats was extensively metabolized to radioactive taurine. It therefore appears that the cat and to a lesser extent, the guinea pig, have transamidinase or amidinohydrolase activity for which GES is a substrate. However, this substance rapidly depletes taurine levels in the omnivores studied, and promises to be useful in further investigations on taurine in these species.

Taurine mobilizing effects of beta alanine and other inhibitors of taurine transport

Oral administration of a 3% beta alanine solution in the drinking water was as effective in increasing urinary taurine excretion and decreasing tissue taurine levels in rats as subcutaneous or intraperitoneal administration. Beta alanine was more effective in reducing tissue taurine levels in rats and guinea pigs than in mice. Other inhibitors of taurine transport were compared with beta alanine for their ability to reduce tissue taurine levels. Taurocyamine, the guanidino analogue of taurine, was less effective in rats than beta alanine in reducing taurine levels in gastrocnemius but more effective in reducing brain taurine levels, whereas the homologue of beta alanine, GABA, was relatively ineffective in either mice or rats.

Pilot studies on membranes and some transport mechanisms in Friedreich's ataxia.

The observed anomalies in high density lipoproteins in Friedreich's ataxia led us to investigate the state of cellular membranes in this illness. As a preliminary screening program, we studied the shape of erythrocytes; the phospholipid content of platelets and the transport properties of these membranes as indirectly reflected in the absorption of Vit E and the renal handling of orally injected taurine. All these investigations were normal, except for a tendency towards more echinocytes in Friedreich's ataxia and the insignificant increase in taurine urinary excretion after an oral load. We concluded that the possible membrane abnormalities are not major and will have to be searched for with more subtle and specific tests.

Simplified two-step column-chromatographic determination of taurine in urine.

A two-step column-chromatographic procedure for accurate and rapid determination of taurine in urine is described. Sulfosalicyclic-acid deproteinized samples are chromatographed on a 0.9 X 10 cm column of cation-exchange resin (AG 50W-XB), with use of a pH 2.2 sodium citrate eluting buffer such that taurine and the more highly acidic compounds in urine are eluted in the void volume, and then on a 0.9 X 8 cm column of anion-exchange resin (AG 2-X8), from which taurine is preferentially eluted with 1 mol/liter acetic acid. The color developed with ninhydrin is directly proportional to taurine amounts as low as 0.01 mumol/sample. The method is highly reproducible, with analytical recoveries greater than 95%. The presence of 333 mumol of urea and 1 mumol of cysteic acid did not interfere in the analysis. When a mixture of C14-labeled amino acids other than taurine were co-chromatographed with taurine, less than 2% of the total counts loaded were located in the taurine fraction. Values for urinary taurine excretion by rats according to the present method agreed well with values obtained with an automated amino acid analyzer. Advantages of the present method for the determination of taurine are discussed.

Dietary-Induced Variations in Urinary Taurine Levels of College Women

Dietary-induced variations in the urinary taurine excretion of healthy college women were investigated. Data were collected in three metabolic studies in which nutritionally adequate diets of constant composition were fed. Variables included isonitrogenous natural food and semi-purified diets; taurine, cystine and meat supplements; and kind and amount of dietary fat. Observed urinary taurine levels were low and ranges were narrower than those reported by other investigators. The low taurine excretion at the completion of the studies was considered evidence that urinary taurine levels in humans is related to the level of body taurine as well as to the level of dietary taurine. Urinary taurine excretion was shown to be related to dietary taurine intake rather than protein (nitrogen) intake. A relationship between kind of dietary fat and taurine excretion is suggested.

101: Sulfate and taurine urinary excretion in hypothalamo-hypophyseal dwarfs /HSD/ before and after HGH treatment

The up-take of sulfates by growing cartilage is on the high level. Cysteine /Gaull et al,; Raiha, 1971/ and homocysteio acid /MoCully, 1971/ are the main sources of active sulfate. In order to see if growth hormone interferes with metabolic steps initiating cartilage growth the study of urinary sulfate and taurine excretion has been performed in 17-hypothalamo-hypophyseal dwarfs /HSD/, aged 6-15 yrs. 7 of them have subsequently been treated with 6 mg/week of HGH. After 3 days of standard diet average from 3 days sulfate S in the urine was 234,2 ± 94,9 mgs S/day and taurine excretion 292,8 ± 122,6 μM/day in 9 normal controls. In 17 HSD the same values were 522,3 ± 27,3 mgs S/day /P(0,001/ and for taurine /n=5/ 302,4 ± 258,4 μM/Aay /P>0,5/. After 4-6 week HGH therapy the respective values were: 320,2 ± 113,8 mgs S/day for sulfates /P<0,005/ and 626,8 ± 197,6 μM/day for taurine /0, 1 < p>0,05/. Cysteine oral loading /0,130 g/kg/day during 3 days/ increased sulfate excretion in the urine in HSD, but methionine /0,225 g/kg/day/ did it to the lesser degree. HGH treatment increased in HSD taurine excretion and considerably diminished urine sulfate. The effect is more pronounced after methionine. HGH might activate the oxidation of cystelne from methionine precursor.