Nutritional Taurine Deficiency and Feline Pregnancy and Outcome

Author(s):  
J. A. Sturman ◽  
T. Palackal ◽  
H. Imaki ◽  
R. C. Moretz ◽  
J. French ◽  
...  
Keyword(s):  
1984 ◽  
Vol 19 (4) ◽  
pp. 462-466 ◽  
Author(s):  
Arthur Cooper ◽  
James M. Betts ◽  
Gilberto R. Pereira ◽  
Moritz M. Ziegler

2002 ◽  
Vol 282 (5) ◽  
pp. C1113-C1120 ◽  
Author(s):  
Stephen W. Schaffer ◽  
Viktoriya Solodushko ◽  
David Kakhniashvili

Cellular sodium excess is cytotoxic because it increases both the intracellular osmotic load and intracellular calcium concentration ([Ca2+]i). Because sodium levels rise during hypoxia, it is thought to contribute to hypoxic injury. Thus the present study tested the hypothesis that taurine-linked reductions in [Na+]i reduce hypoxia-induced cell injury. Taurine depletion was achieved by exposing isolated neonatal cardiomyocytes to medium containing the taurine analog β-Alanine. As predicted, the β-Alanine-treated cell exhibited less hypoxia-induced necrosis and apoptosis than the control, as evidenced by less swelling, shrinkage, TdT-mediated dUTP nick end labeling staining, and accumulation of trypan blue. After 1 h of chemical hypoxia, [Na+]i was 3.5-fold greater in the control than the taurine-deficient cell. Although more taurine was lost from the control cell than from the β-Alanine-treated cell during hypoxia, the combined taurine and sodium osmotic load was lower in the β-Alanine-treated cell. Taurine deficiency also reduced the degree of hypoxia-induced calcium overload. Thus the observed resistance against hypoxia-induced necrosis and apoptosis is probably related to an improvement in sodium and calcium handling.


2021 ◽  
Vol 7 ◽  
Author(s):  
Tammy J. Owens ◽  
Andrea J. Fascetti ◽  
C. Christopher Calvert ◽  
Jennifer A. Larsen

Whole-prey diets for exotic feline species are common, and this practice has also increased in popularity for domestic cats. However, prior analyses of prey indicate possible essential amino acid inadequacy, and dilated cardiomyopathy from taurine deficiency was reported in cats fed whole ground rabbit. Crude protein, body water, and amino acid concentrations were evaluated in fresh and frozen ground rabbits with (n=10) or without (n = 10) gastrointestinal tracts. Amino acids were greater in fresh samples without gastrointestinal tracts (p < 0.05) except taurine, glycine, and cysteine. When normalized for protein content, only glutamate, alanine, methionine, isoleucine, tyrosine, lysine, histidine, and arginine were greater in fresh rabbits without gastrointestinal tracts (g/16 g N basis; p < 0.05). Freezing at −18°C for 30 days had no effect on crude protein or body water content. After freezing, only methionine was lower and only proline was higher when gastrointestinal tracts were omitted (g/16 g N basis; p < 0.05). Regardless, all essential amino acids except taurine exceeded Association of American Feed Control Officials and National Research Council nutrient recommendations for all feline life stages. In contrast, there was minimal impact of treatment on taurine concentrations. However, although feline taurine requirements for prey and other raw or fresh food diets remain undefined, none of the rabbit samples met any recommendation for taurine concentrations for commercial canned or dry extruded diets, ranging from 20 to 90% of the minimum values. Taurine supplementation is recommended when feeding rabbit to cats. Determination of taurine requirements of cats fed whole-prey diets is warranted.


Aquaculture ◽  
2016 ◽  
Vol 451 ◽  
pp. 254-265 ◽  
Author(s):  
Guillaume P. Salze ◽  
Elizabeth Spangler ◽  
Paul A. Cobine ◽  
Melanie Rhodes ◽  
D. Allen Davis
Keyword(s):  

Author(s):  
Xiaobin Han ◽  
Takashi Ito ◽  
Junichi Azuma ◽  
Stephen W. Schaffer ◽  
Russell W. Chesney

J ◽  
2018 ◽  
Vol 1 (1) ◽  
pp. 57-70
Author(s):  
Takashi Ito ◽  
Shigeru Murakami ◽  
Stephen Schaffer

Taurine, which is abundant in mammalian tissues, especially in the heart, is essential for cellular osmoregulation. We previously reported that taurine deficiency leads to changes in the levels of several metabolites, suggesting that alterations in those metabolites might compensate in part for tissue taurine loss, a process that would be important in maintaining cardiac homeostasis. In this study, we investigated the molecular basis for changes in the metabolite profile of a taurine-deficient heart using pathway analysis based on the transcriptome and metabolome profile in the hearts of taurine transporter knockout mice (TauTKO mice), which have been reported by us. First, the genes associated with transport activity, such as the solute carrier (SLC) family, are increased in TauTKO mice, while the established transporters for metabolites that are elevated in the TauTKO heart, such as betaine and carnitine, are not altered by taurine deficiency. Second, the integrated analysis using transcriptome and metabolome data revealed significant increases and/or decreases in the genes involved in Arginine metabolism, Ketone body degradation, Glycerophospholipid metabolism, and Fatty acid metabolism in the KEGG pathway database. In conclusion, these pathway analyses revealed genetic compensatory mechanisms involved in the control of the metabolome profile of the taurine-deficient heart.


PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0210233
Author(s):  
Joanna L. Kaplan ◽  
Joshua A. Stern ◽  
Andrea J. Fascetti ◽  
Jennifer A. Larsen ◽  
Hannah Skolnik ◽  
...  

2006 ◽  
Vol 136 (10) ◽  
pp. 2502-2505 ◽  
Author(s):  
Kwang Suk Ko ◽  
Cristina L. Tôrres ◽  
Andrea J. Fascetti ◽  
Martha H. Stipanuk ◽  
Lawrence Hirschberger ◽  
...  

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