Low plasma taurine concentration in Newfoundland dogs is associated with low plasma methionine and cyst(e)ine concentrations and low taurine synthesis (original) (raw)
Related papers
Journal of Animal Physiology and Animal Nutrition, 2003
Taurine (Tau) deficiencies have been associated with the feeding of commercial lamb-meal and rice diets to dogs. We hypothesized that the poor digestibility of some lamb-meals may limit sulphur amino acids availability for Tau synthesis and/or increase of Tau degradation in the gut. Growing dogs were fed either a lamb-meal-based (Diet A) or poultry byproduct-based (Diet B) commercial diet. Plasma, whole blood and urinary Tau were measured for 22 weeks. Plasma and whole blood Tau concentrations were similar between the groups throughout the study. Urinary excretion of Tau in dogs fed diet A was 3.2 times greater than that from dogs fed Diet B, suggesting greater renal reabsorption and the need for conservation of Tau in the Diet A group. Food restriction affected Tau status as indicted by a positive correlation of food intake and urinary Tau. Dogs fed Diet A were given antibiotics to inhibit bacterial activity in the gut. Increases in breath hydrogen, indicative of increased bacterial activity, correlated negatively with urinary Tau. Urinary Tau increased by 54% when methionine (Met) was supplemented to Diet A, supporting the suggestion of a low bioavailability of sulphur amino acids and/or an increased fecal loss of Tau in dogs consuming Diet A.
Plasma Taurine Concentrations in Normal Dogs and in Dogs With Heart Disease
Journal of Veterinary Internal Medicine, 1995
Plasma taurine concentrations were determined in 76 dogs with dilated cardiomyopathy (DCM), 28 dogs with acquired valvular disease (AVD), and 47 normal (control) dogs. The data were collected at 2 referral centers, The Animal Medical Center, New York, NY (AMC), and the University of California, Davis (UCD), and the studies were conducted independently. Different anticoagulants (sodium citrate at AMC and lithium heparin at UCD) were used to collect the plasma samples. Paired analysis of samples showed a significant difference in plasma taurine concentrations, depending on the anticoagulant used. Consequently, results from each clinic were analyzed separately. Plasma taurine concentrations were significantly higher in dogs with AVD (median, 133 nmol/mL; range, 25 to 229 nmol/mL) than in control dogs (median, 63 nmol/ml; range 44 to 224 nmol/mL) and dogs with DCM (median, 72 nmol/ mL; range, 1 to247 nmol/mL) at AMC (P< .001). Thenumber of dogs with AVD at UCD was too small to draw meaningful conclusions. At UCD, the median plasma taurine concentration was 98 nmol/mL (range, 28-1 69 nmol/mL) aurine (Zaminoethane sulfonic acid) is the most abun-
Plasma and whole blood taurine in normal dogs of varying size fed commercially prepared food
Journal of Animal Physiology and Animal Nutrition, 2003
The objective of the present study was to examine the effect of signalment, body size and diet on plasma taurine and whole blood taurine concentrations. A total of 131 normal dogs consuming commercially prepared dog food had blood drawn 3-5 h postprandially to be analysed for plasma amino acids and whole blood taurine. Body weight and morphometric measurements of each dog were taken. Plasma and whole blood taurine concentrations were 77 ± 2.1 nmol/ml (mean ± SEM) and 266 ± 5.1 nmol/ml (mean ± SEM), respectively. No effect of age, sex, body weight, body size, or diet was seen on plasma and whole blood taurine concentrations. Mean whole blood taurine concentrations were lower in dogs fed diets containing whole grain rice, rice bran or barley. The lowest whole blood concentrations were seen in dogs fed lamb or lamb meal and rice diets. Plasma methionine and cysteine concentrations were lower in dogs fed diets with animal meals or turkey, and whole grain rice, rice bran or barley. Fifteen of 131 dogs had plasma taurine concentrations lower than, or equal, to the previously reported lowest mean food-deprived plasma taurine concentration in normal dogs of 49 ± 5 nmol/ml (mean ± SEM) . These findings support the theory that taurine deficiency in dogs may be related to the consumption of certain dietary ingredients. Scientific and clinical evidence supports the hypothesis that dilated cardiomyopathy is associated with low blood taurine concentration in dogs; therefore, further work is indicated to determine the mechanism by which diet can affect taurine status in dogs.
Taurine deficiency and dilated cardiomyopathy in golden retrievers fed commercial diets
PLOS ONE
Introduction Golden retrievers are over-represented in cases of taurine-deficient dilated cardiomyopathy and recently a surge in cases has prompted further investigation. Objective To describe the clinical, dietary, and echocardiographic features in golden retrievers diagnosed with taurine deficiency and dilated cardiomyopathy, and to determine specific dietary associations. A second aim was to determine the whole blood taurine concentrations in a representative sample of healthy golden retrievers. Animals Twenty-four client-owned golden retrievers with documented taurine deficiency and dilated cardiomyopathy and 52 healthy client-owned golden retrievers.
Journal of Veterinary Internal Medicine, 1997
Fourteen American Cocker Spaniels (ACS) with dilated cardiomyopathy (DCM) were studied to determine if individuals of this breed with DCM are systemically taurine-or carnitinedeficient and to determine if they are responsive to taurine and carnitine supplementation. American Cocker Spaniels with DCM were identified using echocardiography, and plasma was analyzed for taurine and carnitine concentrations. Each dog was randomly assigned to receive either taurine and carnitine supplementation or placebos. Echocardiograms and clinical examinations were repeated monthly for 4 months. During this period, the investigators and owners were blinded with respect to the treatment being administered. Each dog was weaned off its cardiovascular drugs (furosemide, digoxin, and an angiotensin converting enzyme inhibitor) if an echocardiographic response was identified. At the 4-month time period, each investigator was asked to decide whether he or she thought his or her patient was receiving placebo or taurine/ carnitine, based on presence or absence of clinical and echocardiographic improvement. Unblinding then occurred, and dogs receiving placebos were switched to taurine and carnitine supplementation and followed monthly for 4 additional months.
Taurine deficiency in Newfoundlands fed commercially available complete and balanced diets
Journal of the American Veterinary Medical Association, 2003
Objective—To determine taurine status in a large group of Newfoundlands related by environment, diet, or breeding to a dog with dilated cardiomyopathy and taurine deficiency. Design—Prospective study. Animals—19 privately owned Newfoundlands between 5 months and 11.5 years old that had been fed commercial dry diets meeting established nutrient recommendations. Procedure—Diet histories were obtained, and blood, plasma, and urine taurine concentrations and plasma methionine and cysteine concentrations were measured. In 8 dogs, taurine concentrations were measured before and after supplementation with methionine for 30 days. Ophthalmic examinations were performed in 16 dogs; echocardiography was performed in 6 dogs that were taurine deficient. Results—Plasma taurine concentrations ranged from 3 to 228 nmol/mL. Twelve dogs had concentrations < 40 nmol/mL and were considered taurine deficient. For dogs with plasma concentrations < 40 nmol/mL, there was a significant linear correlat...
Taurine-Deficient Dilated Cardiomyopathy in a Family of Golden Retrievers
Journal of the American Animal Hospital Association, 2005
A reversible taurine-deficient dilated cardiomyopathy occurred in five related golden retrievers. An apical systolic heart murmur was the most common physical abnormality. According to fractional shortening and end-systolic diameter on echocardiography, significant improvements (P<0.005) were recorded within 3 to 6 months of starting taurine supplementation. The dogs regained substantial systolic function, and four were weaned off all cardiac medications except taurine. This response to therapy was unusual, because canine dilated cardiomyopathy is generally progressive and fatal.
Taurine's role in clinical practice
Journal of Small Animal Practice, 1990
Dilated cardiomyopathy has been recognised as a significant heart disease and cause of death in pet cats in the United States. The cause of dilated cardiomyopathy which was unknown and the prognosis grave. An association between low plasma taurine concentrations and dilated cardiomyopathy was established. Daily administration of taurine (250-1000 mg) orally increased plasma taurine concentrations and reversed the clinical signs. It was previously thought that cats became taurine deficient when fed commercial dog food or unbalanced home-cooked diets. We found a high association between the type of diet fed, plasma taurine concentrations and the incidence of myocardial failure and feline central retinal regeneration. Many commercial cat foods were found to cause taurine depletion associated with myocardial failure or central retinal degeneration. It is now established that taurine deficiency is a major cause of myocardial failure in cats and that modification of commercial cat food formulations with regard to taurine content has resulted in a dramatic decrease in the incidence of dilated cardiomyopathy in cats in the United States.