by Kevin Tan (42761646)
Sweetness is one of the tastes that our tongue can recognise. Sweetness is always associated with a lot of things, like sugar, energy, carbohydrate, obesity and etc. Almost all people around the world have tasted sweetness in the food they eat. However, cats cannot taste sweetness in every single food that they eat. Therefore, cat has no preference on any sweet stuff such as candy, etc. A sweets stuff will taste plain on them, it was proved in the Li X, et al. (2005)’s experiment when they tried to give to sweetened water and plain water and the cat has no any preference on both.
In mammals, the receptor to recognise sweetness is formed by dimerization of two proteins which are Tas1r2 and Tas1r3 (Li X, et al. 2005). Both proteins were examined by Li X et al. (2005) and they found that Tas1r3 was gene functionally same with other animals but it was not in Tas1r2 gene. Tas1r2 gene has 247 base pair microdeletion in exon 3 and it also stops codons in exons 4 and exons 6 (Li X, et al. 2005). Therefore, the insensitiveness of the cats towards sweets is caused by dysfunction of Tas1r2 gene which play important role for detecting sweetness. The dysfunction of Tas1r2 gene is called as a pseudogene. In addition, cat has a response to another taste like salty, sour, bitter but only sweet taste that can be recognised by its. The disorder of responding to sweetness in cat also admitted by Biello (2007), that he said the Tas1r2 gene is not coded by proper protein so it does not allow cat to taste sweets.
Source: Li X, Li W, Wang H, Cao J, Maehashi K, et al. 2005
On the other hand, an interesting result was found by further experiment. Cat, besides lacking at tasting sweet things, they also lack of glucokinase in their livers (Biello, 2007). Glucokinase is an enzyme that is located in pancreas cell that has a function to phosphorylate glucose (Gloyn 2003). Dottie (2010) also stated that cat is lacking of glucokinase for phosphorylating the glucose inside the cells and this is also admitted by Myers and Klasing (1999). Therefore, to fulfil their body need due to phosphorylating glucose, cat release more hexokinase to replace glucokinase (Dottie 2010). However, hexokinase works less efficiently than glucokinase. In cats the amount of hexokinase is huge compare to other animals (Dottie 2010). Therefore, cat is highly risk to suffer either diabetes or obesity due to inefficiency to breakdown glucose. Dottie (2010) also stated if cats are being fed with high carbohydrate foods, it might raise their possibility to get diabetes.
To conclude, cat cannot differentiate between plain tastes with sweets taste, this thing happen due to the dysfunction of Tas1r2 gene which one of two genes to recognise sweetness. Moreover, the lack of ability to taste sweetness also been followed by the lack of glucokinase. Therefore, cats’ pancreas will take longer to breakdown glucose and this can lead them to obesity or diabetes if they keep fed by highly carbohydrate food.
Biello, D 2007, Strange but True: Cats Cannot Taste Sweets, media release, 16 August 2007, Scientific AmericanTM, viewed 16 March 2012, <http://www.scientificamerican.com/article.cfm?id=strange-but-true-cats-cannot-taste-sweets>.
Gloyn, AL 2003, ‘Glucokinase (GCK) mutations in hyper- and hypoglycemia: maturity-onset diabetes of the young, permanent neonatal diabetes, and hyperinsulinemia of infancy’, Human Mutation, vol. 22, no. 5, pp. 353-362, < http://www.ncbi.nlm.nih.gov/pubmed/14517946>.
Laflamme, DP 2010, ‘Cats and Carbohydrates: Implication for Health and Disease’, Focus on Nutrition, viewed 16 March 2012, < http://cp.vetlearn.com/Media/PublicationsArticle/PV0110_laflamme.pdf>.
Li X, Li W, Wang H, Cao J, Maehashi K, et al. 2005, ‘Pseudogenization of a Sweet-Receptor Gene Accounts for Cats' Indifference toward Sugar. Viewed 16 March 2012, PLoS Genet 1(1): e3. doi:10.1371/journal.pgen.0010003.
Myers, MR & Klasing KC 1999, ‘Low Glucokinase Activity and High Rates of Gluconeogenesis Contribute to Hyperglycemia in Barn Owls (Tyto alba) after a Glucose Challenge’ vol. 129, no. 10, pp. 1896-1904, viewed 16 March 2012, < http://jn.nutrition.org/content/129/10/1896.full>.