1. What is taurine?
2-aminoethanesulfonic acid, or better known as taurine is an organic compound and amino acid naturally found in animal-based products like meat, fish, eggs, and dairy. It is synthesized from an amino acid called cysteine in most species. However, taurine is considered an essential amino acid for feline species, meaning that they are not able to synthesize it in sufficient quantities.
Taurine is the only source that’s used to conjugate bile acids in the feline metabolism, contributing to taurine deficiency susceptibility even further. Taurine deficiency in cats has several consequences, of which some can be fatal. Therefore, cats need to acquire it from dietary sources and external supplements (Zoran, 2002).
2. Taurine metabolism in the body
In cats, the overall metabolism of taurine is made up of 3 parts: synthesis, absorption, and excretion (Lambert et al, 2014).
2.1. Absorption and distribution
Dietary taurine is absorbed from the small intestines into the bloodstream through TauT- and PAT1-transporters. TauT-transporters are Na+ - and Cl -dependent, while the PAT1-transporters are pH-dependent. They are primarily found in the plasma membrane (Lambert et al, 2014). Taurine uptake is inhibited by guanidinoethyl sulfonate (GES), β-alanine, and GABA (Ripps and Shen, 2012).
From the bloodstream, taurine is yet again transported by TauT and PAT1 to the tissues. Most of the taurine is distributed to tissues with metabolic activity (Lambert et al, 2014).
2.2. Excretion
Taurine can either be eliminated through the kidneys as urine or it can be conjugated into bile acids and thus leave with the feces (Lambert et al, 2014). Since cats conjugate bile acids only with taurine, this contributes to a massive loss of this essential amino acid (Zoran, 2002).
The excretion of taurine is proportional to the dietary intake of taurine. As taurine intake increases, the excretion will increase accordingly. This regulation will take place within days after increased dietary taurine supply. However, only a longer period of modified taurine intake will lead to changes in the taurine concentration of the plasma (Lambert et al, 2014).
2.3. Synthesis
The main location of taurine synthesis is in the liver. The liver reacts to the increased or decreased cysteine intake and adapts the taurine synthesis accordingly. Other locations of synthesis are present in the skeletal muscle, adipose tissue, mammary glands, brain, and lungs (Lambert et al, 2014).
Taurine is mainly derived from the amino acids methionine and cysteine (Zoran, 2002). The synthesis of taurine from these amino acids requires the presence of the enzymes cysteine dioxygenase (CDO) and cysteine sulfinate decarboxylase (CSAD). As a result, cysteine sulfinate and hypotaurine are formed, and finally taurine through an oxidation reaction (Lambert et al, 2014). However, these enzymes have particularly low activity in feline species, which in turn affects the synthesis accordingly (Zoran 2002).
Another known pathway for taurine synthesis is mediated by the breakdown of coenzyme A to cysteamine. Cysteamine is then oxidized by cysteamine dioxygenase, resulting in hypotaurine (Lambert et al, 2014).
Figure 1. Taurine synthesis from cysteine and coenzyme A (Lambert et al, 2014)
3. Physiological roles
3.1. Cardiovascular
The importance of taurine in cardiovascular organ systems has been proved through its particularly high concentration in cardiac and skeletal muscle. Therefore, it has been suggested that the high taurine concentration correlates with a high heart rate and the workload of the heart.
Taurine is essential in maintaining a physiological contractile function in the muscles by the regulation of Ca2+ -sensitive transporters and myofibrils. This particularly has been seen as one of the most prominent reasons for heart failure. Taurine alters the Ca2+ -transport in the sarcoplasmic reticulum through two pathways.
1) Phosphorylation of phospholamban, the sarcoplasmic reticular phosphoprotein, upregulates the rate of Ca2+- influx to the sarcoplasmic reticulum. Thus, the relaxation of the myocardium is increased. This phosphoprotein is highly taurine-dependent, and the lack of taurine will therefore lead to a decrease in myocardial relaxation.
2) The antioxidative properties of taurine also affect the Ca2+ -transport and thus the contractile features of the muscles. This has been proven through the inhibition of sarcoplasmic reticular Ca2+ ATPase by oxidative stress.
The lack of taurine also leads to increased phosphorylation of troponin I. This inhibits the binding of Ca2+ to troponin and thus inhibits cardiomyocyte contraction. It has also been noted that decreased taurine concentration correlates with apoptosis of cardiac muscle cells and therefore the loss of the heart muscle cells (Schaffer et al, 2010).
3.2. Ophthalmic systems
Taurine is found in high amounts in the ocular tissues due to the presence of TauT-transporters (Ripps and Shen, 2012). Therefore taurine deficiency affects the vision in many ways.
Taurine deficiency decreases the amplitude of the b-wave in the measurement of electric activity of the retina. It also degenerates the photoreceptors, affecting the cones to a higher degree. It has also been noted that taurine deficiency correlates with the disturbance of the feline characteristic structure, the tapetum lucidum. This will interfere with the light reflection of the eye (Schaffer et al, 2013). Taurine also plays an important role in protecting ganglion cells from apoptosis (Ripps and Shen, 2012). All these above-mentioned taurine-connected factors contribute to the dysfunction of the vision.
3.3. Development
Taurine deficiency leads to smaller body and brain weight, abnormalities in the visual sensory organs, and defected mitochondrial effects. (Lambert et al, 2014)
Taurine has a major role in brain development in both embryos and adults. Lack of taurine delays the differentiation and migration of the cells in multiple areas of the brain. It has also been noted that taurine activates stem cell precursors of neurons to differentiate into neurons instead of glial cells (Ripps and Shen, 2012).
4. Chemical background
Taurine, also known as 2-aminoethanesulfonic acid is an amino acid with a sulfonate group. However, it lacks the carboxyl group, which is characteristic of amino acids (Ripps and Shen, 2012). It also does not participate in forming of the peptide bond. Taurine is an essential amino acid that is synthesized from cysteine and methionine (Schaffer et al, 2010). Taurine can be found in all cells and is particularly concentrated in tissues with electrical excitability, such as the brain, the retina of the eye, the heart, and skeletal muscles (Oja et al, 2007).
Taurine is a stable compound and can be seen as an optimal substance taking part in many basic processes in the body (Schaffer et al, 2010). It is slightly acidic and is therefore a hydrophilic molecule with the inability to permeate biological membranes (Lambert et al, 2014). Some of its roles are maintaining normal contractile functions, working as an osmoregulator, stabilizing membrane, indirectly regulating oxidative stress, eliminating toxins from the body, and metabolism of lipids (via bile acid conjugation). (Schaffer et al, 2010, Lambert et al, 2014)
5. Taurine in domestic cats’ diet
Taurine is a β-sulphonic amino acid synthesized in animals from dietary sulfur amino acids. Felines require adequate amounts of taurine to maintain their health and avoid deficiency problems. Concentrations of taurine in healthy cats are >300 nmol/mL, while concentrations <160 nmol/mL easily result in deficiency (Zoran, 2002).
Taurine is found in animal origin food sources, mainly in meat, but also in egg, dairy, and bone. Unlike many mammals, felines do not synthesize citrulline and have a particularly restricted ability of taurine synthesis from cysteine (Che et al, 2021). This makes it crucial for them to consume animal-based proteins to avoid deficiency. Thus, when plant-based proteins are used in the diet, supplements are needed (Zoran, 2002). Taurine must be provided regularly since it cannot be stored in large amounts. The supplied taurine is also utilized faster than its replenished.
All the essential amino acids including taurine should be included in diets of felines. They are particularly sensitive to deficiencies regarding arginine and taurine. These conditions can rapidly result in hyperammonemia and retinal damage (Che et al, 2021).
6. Taurine Deficiency
Many studies show that taurine deficiency has a lot of effects on different species and breeds of animals during different stages of life. While American Cocker Spaniels are more likely to face dilated cardiomyopathy due to taurine deficiency compared to other canine breeds (Gavaghan and Kittleson, 1997), infant monkeys are more likely to have growth depression (Hayes and Stephan, 1980) while adults seem to tolerate it much better. Taurine deficiency in humans has its own effects as well.
The situation is way more concerning when it comes to our feline companions. Taurine deficiency occurs in a large number of cats fed unfortified commercial diets. Deficiency arises because cats are unable to absorb all the taurine in processed diets and since they are not capable of synthesizing taurine either, it is rather hard for them to close the gap between the absorbed amount and the required amount. This makes taurine an essential amino acid for domesticated cats and their wild relatives alike. Cats with taurine deficiency are more likely to develop retinal degeneration, cardiomyopathy, and have growth and development problems. Taurine deficiency can be measured from plasma concentration of taurine with 30 mmol/l being the crucial minimum. (Hayes, 1989). While the consequences of deficiency are rather serious, clinical signs are rather slow to develop. Thankfully, if caught in earlier stages, taurine deficiency is usually treatable with supplements.
The main areas taurine deficiency in cats affects cardiovascular and ophthalmic functions and pathologies, as well as birth and developmental defects.
6.1. Cardiovascular Defects
One of the main research areas related to pathologies due to taurine deficiency is certainly its cardiovascular effects. “Several species, among them cats, dogs, and foxes, develop cardiomyopathies when maintained on a taurine deficient diet.” (Schaffer, 2010)
With the help of ECG-based evidence, the association between cardiomyopathy and low plasma taurine concentrations in domestic cats has only gotten clearer. Cardiomyopathy is the weakening of the muscle cells of the heart and due to this enlargement in the heart muscle, the heart cannot pump blood effectively. This condition is fortunately reversible by nutritional taurine therapy if treated in time. (Sturnman, 1992) The aforementioned studies have led commercial cat foods to be fortified with taurine and eventually produce taurine supplements for cats as well.
As further studies were being conducted, scientists noticed that there were cats that still had taurine deficiency, even if they were fed the proper amount of taurine in their diets. Which led them to further investigate what could be coupling with taurine in the cat’s metabolism. According to a study conducted by Dow and Fettman in 1992, "Taurine depletion and cardiovascular disease (cardiomyopathy and thromboembolism) developed unexpectedly in 3 of 6 healthy adult cats during a potassium-depletion study", showing the clear importance of potassium and taurine balance in cats. (Dow and Fettman, 1992) Nowadays most taurine supplements for cats are also fortified with potassium for this very reason.
6.2. Ophthalmic Defects
Retinopathies due to taurine deficiency have been investigated rather intensively over the years. “Although it has been known for many years that cats are susceptible to central retinal degeneration, the cause was only recognized to be taurine deficiency in 1975”. (Sturman, 1992) Which has led to further investigations in this area.
According to K.C. Hayes, DVM, PhD, the primary defect appears to be in the photoreceptor cell’s outer segments and the underlying structure of the feline characteristic, tapetum lucidum. If the retinal tissue’s taurine concentration falls below 50 to 70% of its normal value, the structure and function of the retina decline accordingly. However, if taurine supplementation is put in place within the cat’s diet, this deterioration can be corrected. Without the supplementation, the photoreceptor cells eventually die and disappear, resulting in irreparable damage and eventually causing blindness. “Sadly, some lesions cannot be reversed even with proper taurine supplementation, but the remaining retina could be saved from further damage”. (Hayes, 1982)
6.3. Birth and Developmental Defects
Taurine is considered essential for all life stages of cats. According to Cross Road Animal Hospital in California, kittens born to mothers with this sort of deficiency face lots of growth problems and might end up being exposed to bone fractures.
Taurine deficiency leads to a smaller birth weight in both cats (Sturman 1991) and rodents (Ejiri et al. 1987). The offspring of cats reared on a taurine-free diet exhibit profound developmental abnormalities, among these being: smaller body weight, smaller brain weight, abnormal hind leg development as well as a degeneration or abnormal development of the retina and visual cortex (Sturman 1991).
7. Conclusion
To sum up, taurine is an irreplaceable part of the feline diet, and considering the aforementioned effects of taurine deficiency, it is clear that taurine supplementation is important in the domestic cat’s diet. Since fortified diets are not always enough for some of our cat companions, it would only help to give them more taurine supplements to supplement their heart, eye, and renal health, as well as their overall development.
References
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Dow, S.W.; Fettman, M. J.; Smith, K. R.; Ching, S.V.; Hamar, D.W.; Rogers, Q. R. (1992). Taurine depletion and cardiovascular disease in adult cats fed a potassium-depleted acidified diet. Am J Vet Res 53: (3) 402-5.
Ejiri, K.; Akahori, S.; Kudo, K.; Sekiba, K.; Ubuka, T. (1987). Effect of guanidinoethyl sulfonate on taurine concentrations and fetal growth in pregnant rats. Biol Neonate 51: 234-240.
Gavaghan, B. J.; Kittleson, M.D. (1997). Dilated cardiomyopathy in an American cocker spaniel with taurine deficiency. Aust Vet J75: 862–868
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Lambert, I. H.; Kristensen, D. M.; Holm, J. B.; Mortensen, O. H. (2014): Physiological role of taurine - from organism to organelle. Acta Physiol 213: 191-212
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Ripps, H.; Shen, W. (2012). Review: taurine: a "very essential" amino acid. Molecular vision 18: 2673–2686.
Schaffer, S.W.; Jong, C. J.; KC, R.; Azuma J. (2010). Physiological roles of taurine in heart and muscle. Journal of Biomed Science 17: (S2)
Schaffer, S.W.; Jong, C. J.; Warner, D.; Ito, T.; Azuma, J. (2013). Taurine Deficiency and MELAS Are Closely Related Syndromes. Advances in Experimental Medicine and Biology 776: (Taurine 8) 153-165.
Sturman, J.A. (1991). Dietary taurine and feline reproduction and development. J Nutr. 121: (11) 166–S170.
Sturman, J. (1992). Review: Taurine Deficiency and the Cat. Advances in Experimental Medicine and Biology 315.
Zoran, D. L. (2002). The carnivore connection to nutrition in cats. Journal of the American Veterinary Medical Association, 221: (11) 1559-1567
Figure references
Figure 1: Lambert, I. H.; Kristensen, D. M.; Holm, J. B.; Mortensen, O. H. (2014): Physiological role of taurine - from organism to organelle. Acta Physiol 213: 191-212