ArticlePDF AvailableLiterature Review

Cats Lack a Sweet Taste Receptor

Authors:

Figures

Content may be subject to copyright.
Cats Lack a Sweet Taste Receptor
1,2,3
Xia Li
*
, Weihua Li
*
, Hong Wang
*
, Douglas L. Bayley
*
, Jie Cao
*
, Danielle R. Reed
*
, Alexander
A. Bachmanov
*
, Liquan Huang
*
, Véronique Legrand-Defretin
, Gary K. Beauchamp
*,**
, and
Joseph G. Brand
*,‡
*Monell Chemical Senses Center, Philadelphia, PA 19104
WALTHAM Center for Pet Nutrition, Leicestershire LE14 4RT, UK
**Department of Psychology, School of Arts and Sciences and Department of Anatomy, School of Veterinary
Medicine, University of Pennsylvania, Philadelphia, PA 19104
Department of Biochemistry, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA
19104
Keywords
cat; dog; sweet receptor; taste; pseudogene
Domestic cats (Felis silvestris catus) (herein referred to as “cats”) are neither attracted to, nor
show avoidance of the taste of sweet carbohydrates and high-intensity sweeteners (1-3), yet
they do show a preference for selected amino acids (4), and avoid stimuli that taste either bitter
or very sour to humans (1,4). Consistent with this behavioral evidence, recordings from cat
taste nerve fibers and from units of the geniculate ganglion innervating taste cells demonstrated
responses to salty, sour, and bitter stimuli as well as to amino acids and nucleotides, but showed
no response to sucrose and several other sugars (4-11). The sense of taste in cats appears similar
to that of other mammals with the exception of an inability to taste sweet stimuli.
Because only the sweet taste modality appears absent, we postulated that the defect in cats (and
likely in other obligate carnivores of Felidae) lay at the receptor step, subtending this modality.
The possible defects at the molecular level could range from a single to a few amino acid
substitutions, such as is found between sweet “taster” and “nontaster” strains of mice
(12-14), to more radical mechanisms, such as an unexpressed pseudogene.
To distinguish among these possibilities, we identified the DNA sequences and examined the
structures of the 2 known genes Tas1r2 and Tas1r3 that encode the sweet taste receptor
1
Published in a supplement to The Journal of Nutrition. Presented as part of The WALTHAM International Nutritional Sciences
Symposium: Innovations in Companion Animal Nutrition held in Washington, DC, September 15-18, 2005. This conference was
supported by The WALTHAM Centre for Pet Nutrition and organized in collaboration with the University of California, Davis, and
Cornell University. This publication was supported by The WALTHAM Centre for Pet Nutrition. Guest editors for this symposium were
D’Ann Finley, Francis A. Kallfelz, James G. Morris, and Quinton R. Rogers. Guest editor disclosure: expenses for the editors to travel
to the symposium and honoraria were paid by The WALTHAM Centre for Pet Nutrition.
2
Author disclosure: V.L.D. is an employee of the Masterfoods division of Mars. G.K.B. is on an advisory board to the WALTHAM
Centre. Patents describing the uses of the feline receptors are pending, and name as inventors: X.L., W.L., J.G.B., D.R.R., and A.A.B.
Patents describing the uses of the canine receptors are pending, and name as inventors: X.L., W.L., and J.G.B.
3
Supported in part by The WALTHAM Centre for Pet Nutrition (to X.L. and J.G.B.), and by NIH grants R01DC00882 (G.K.B) and
R03DC05154 (L.H.), and a grant from the National Science Foundation (DBJ-0216310 to N. Rawson). This project was also supported
by a grant from the Pennsylvania Department of Health. The Department specifically disclaims responsibility for any analyses,
interpretations, or conclusions. The funding agencies had no role in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
To whom correspondence should be addressed. E-mail: brand@monell.org.
NIH Public Access
Author Manuscript
J Nutr. Author manuscript; available in PMC 2007 November 5.
Published in final edited form as:
J Nutr. 2006 July ; 136(7 Suppl): 1932S–1934S.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
heteromer T1R2/T1R3 in other mammals. We compared these with the sequence and structure
of the same genes in dogs, humans, mice and rats, all species that respond to sweet stimuli.
Molecular cloning of cat Tas1r3 and Tas1r2
We identified 2 receptor genes, Tas1r3 and Tas1r2, in domestic cats by screening a feline
genomic BAC library and performing PCR with degenerate primers on cat genomic DNA.
Using the same strategy as for the canine genomic BAC library, we also identified the same 2
genes from dogs.
The cat Tas1r3 gene shows high similarity with those of dogs, humans, mice and rats at both
the cDNA (from 74 to 87%) and deduced amino acid level (from 72 to 85%). To confirm the
exon-intron boundaries for cat Tas1r3, we performed both RT-PCR on cDNA from cat taste
bud-containing circumvallate and fungiform papillae and PCR on cat genomic DNA using
intron spanning primers, and compared the cDNA sequence with the genomic sequence (data
not shown). Both the cat Tas1r3 and dog Tas1r3 genes are composed of 6 similarly sized exons
and 5 introns (Fig. 1a). There was nothing within the cat Tas1r3 gene that would suggest that
the cat gene was defective compared with that of the dog.
We defined the exon-intron boundaries of cat Tas1r2 by comparison with known Tas1r2 from
other species, e.g., humans and dogs. Within the sequence of cat Tas1r2, we discovered a
microdeletion of 247 bp in exon 3. This deletion is responsible for a frame shift that results in
a premature stop codon at bp 57-59 of exon 4 (Fig. 1b). By aligning cat Tas1r2 DNA sequences
of exons 4, 5, and 6 with their dog counterparts, we found 4 additional stop codons: 1 in exon
4 due to a deletion at bp 123, and 3 in exon 6 due to a substitution at bp 95 and a deletion at
bp 247 (Fig. 1b). The multiple stop codons indicate that the cat Tas1r2 is a pseudogene. In
spite of using numerous (>70) primers corresponding to the message deduced from the
Tas1r2 gene, we were unable to detect message of cat Tas1r2 from circumvallate and fungiform
taste papillae.
RNA and protein expression
Having detected message from cat Tas1r3 but not from cat Tas1r2 by RT-PCR, we used the
more tissue-specific approaches of in situ hybridization and immunohistochemistry to refine
the search for cat Tas1r2 gene expression. The cat Tas1r3 gene was used as a positive control.
The expression of Tas1r3 but not Tas1r2 in cat circumvallate papillae was confirmed by high-
stringency in situ hybridization (15). To test for the presence of protein, cat circumvallate and
fungiform papillae were exposed to polyclonal antibodies against T1R3 and T1R2. T1R3
labeling was present in the taste buds of circumvallate and fungiform papillae, whereas no
T1R2 labeling was detected (15). These results suggest that Tas1r2 is not transcribed, or, if it
is, it degrades rapidly, perhaps through a nonsense-mediated mRNA decay pathway (16),
preventing synthesis of T1R2 protein.
Confirmation of Tas1r2 sequence in six individual cats, tiger and cheetah
We confirmed the sequence of Tas1r2 in 6 additional unrelated healthy adult domestic cats.
Genomic DNA was amplified by PCR using primers that flanked the deletion and stop codons
of the known cat Tas1r2, and sequenced. In addition, we performed PCR on genomic DNA of
1 tiger (Therion International) and 1 cheetah (a gift from the San Diego Zoo). We found that
Tas1r2 in all 6 cats, the tiger, and the cheetah had the identical 247-bp deletion in exon 3, and
had stop codons at the same positions in exon 4. In exon 6, we found evidence for 2 alleles at
position 93-95 in domestic cats, wherein 2 cats show the stop codon, TGA (homozygotes TGA/
TGA); 1 cat was heterozygote TGA/TGG; and 3 of the domestic cats, the tiger and the cheetah
were homozygotes TGG/TGG. The second exon 6 stop codon is also common to all 3 species
Li et al. Page 2
J Nutr. Author manuscript; available in PMC 2007 November 5.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
(TGA for domestic cats, TAG for tigers and cheetahs). Although the third stop codon of exon
6 at bp 697-699 occurred in all 6 domestic cats, the corresponding region in tigers and cheetahs
could not be amplified by PCR.
These data are consistent with the supposition that cat Tas1r3 is an expressed and likely
functional receptor, whereas cat Tas1r2 is an unexpressed pseudogene.
Sweet taste of cats and dogs
Earlier studies on sweet taste in cats and dogs reported that in contrast to cats, dogs prefer
natural sugars, e.g., sucrose, glucose, fructose, and lactose, but not maltose (17-19). Dogs also
show a preference for sodium cyclamate, but not for sodium saccharin (17,20). These
comparative behavioral data are consistent with data generated from electrophysiological
studies. Boudreau classified part of the cat taste system into several group units (I, II, IIIA, and
IIIB). These cat units have their counterparts in the taste system of dogs (class B, A, C, and D
units). Unlike cat group II units, dog class A units respond to sucrose and fructose (5). By
recording from the chorda tympani nerve, Beidler found that cats do not respond to 0.5 mol/L
sucrose, whereas dogs do (11). Anderson et al. (21) showed that taste nerve fibers responding
to strychnine in dogs also respond to saccharin, which implies that dogs find saccharin aversive.
Overall, cats and dogs respond very differently to sweet-tasting stimuli, although both species
belong to Order Carnivora.
Taste and food selection
Taste receptors reflect a species’ food choices, and the genes encoding these receptors often
show individual variation. These variations may or may not affect taste preference. A textbook
example is the individual variation seen in sensitivity to the bitter compound,
phenylthiocarbamide (PTC). A gene of the human TAS2R family of bitter taste receptors,
TAS2R38, associated with this individual variation, shows 3 coding single-nucleotide
polymorphisms giving rise to 5 haplotypes world-wide, accounting for the 55-85% of the
variance in PTC sensitivity (22). In mice, variation in preference for sweet-tasting stimuli maps
to the gene for T1R3, located within the Sac locus (23,24). This gene is allelic in mice, and
several reports identify a missense mutation (I60T) as being the most likely mutation
accounting for the phenotypic differences (12-14,25). However, the same alleles are not
involved in strain-dependent sweet taste preference in rats (26).
In addition to the modulation of behavior that can be caused by point mutations, more profound
behavioral changes can result from the abolishment of gene function through, for example, the
generation of pseudogenes. An example of this effect in mammalian chemoreception lies
within the large repertoire of olfactory receptor genes. Of the human olfactory receptor genes,
>60% are pseudogenes (27), whereas only 20% are classified as such in mice (27,28).
Strikingly, the accumulation of these olfactory pseudogenes in primates reportedly occurred
concomitant with the acquisition of trichromatic color vision, perhaps reflecting the
overarching behavioral changes that such an acquisition engendered (29). Similar generation
of bitter taste receptor pseudogenes, accompanied by a large number of coding region single
nucleotide polymorphisms, can account for the broad diversity displayed by the bitter taste
receptor family. This diversity may play a role in both species-specific and individually
manifested taste preference (30).
In the extreme case, in which a species fails to respond to stimuli representative of an entire
modality, such as cats with sweet taste, the development of a unique food preference behavior,
based on the remaining taste receptors, might be anticipated. With the exception of the
sweetness modality, the taste system of the cat is organized much like that of most other
mammals; thus, discovering the molecular basis for the lack of response to sweet tasting
Li et al. Page 3
J Nutr. Author manuscript; available in PMC 2007 November 5.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
compounds in cats provides a window on the development of strict carnivorous behavior in
Felidae.
ACKNOWLEDGMENTS
We thank Kirsten J. Mascioli and Minliang Zhou for technical assistance. We acknowledge Dr. Mark Haskins of the
School of Veterinary Medicine, University of Pennsylvania and his laboratory for the procurement of animal tissue
and the dedicated assistance of Patty O’Donnell and Karyn Cullen of that laboratory (NIH grants RR002512 and
DK025759 to M.H.).
LITERATURE CITED
1. Beauchamp GK, Maller O, Rogers JG. Flavor preferences in cats (Felis catus and Panthera sp.). J
Comp Physiol Psychol 1977;91:1118–27.
2. Bartoshuk LM, Jacobs HL, Nichols TL, Hoff LA, Ryckman JJ. Taste rejection of nonnutritive
sweeteners in cats. J Comp Physiol Psychol 1975;89:971–5. [PubMed: 1184803]
3. Carpenter JA. Species differences in taste preference. J Comp Physiol Psychol 1956;49:139–44.
[PubMed: 13319525]
4. White TD, Boudreau JC. Taste preferences of the cat for neurophysiologically active compounds.
Physiol Psychol 1975;3:405–10.
5. Boudreau, J.; White, T. Flavor chemistry of carnivore taste system. In: Society, AC., editor. Flavor
chemistry of animal foods. Washington, DC: 1978. p. 102-28.
6. Boudreau JC, Bradley BE, Bierer PR, Kruger S, Tsuchitani C. Single unit recordings from the
geniculate ganglion of the facial nerve of the cat. Exp Brain Res 1971;13:461–88. [PubMed: 5137297]
7. Boudreau JC, Oravec J, White TD, Madigan C, Chu SP. Geniculate neuralgia and facial nerve sensory
systems. Arch Otolaryngol 1977;103:473–81. [PubMed: 880119]
8. Boudreau JC, Alev N. Classification of chemoresponsive tongue units of the cat geniculated ganglion.
Brain Res 1973;17:157–75. [PubMed: 4709142]
9. Dinger B, Fidone SJ, Stensaas FJ. Gustatory trophic action of arterial chemosensory neurones in the
cat. J Physiol 1984;356:49–64. [PubMed: 6084060]
10. Robinson PP. The characteristics and regional distribution of afferent fibres in the chorda tympani of
the cat. J Physiol 1988;406:345–57. [PubMed: 3254415]
11. Beidler LM, Fishman IY, Hardiman CW. Species differences in taste responses. Am J Physiol
1955;181:235–9. [PubMed: 14376602]
12. Bachmanov AA, Li X, Reed DR, Ohmen JD, Li S, Chen Z, Tordoff MG, de Jong PJ, Wu C, et al.
Positional cloning of the mouse saccharin preference (Sac) locus. Chem Senses 2001;26:925–33.
[PubMed: 11555487]
13. Reed DR, Li S, Li X, Huang L, Tordoff MG, Starling-Roney R, Taniguchi K, West DB, Ohmen JD,
et al. Polymorphisms in the taste receptor gene (Tas1r3) region are associated with saccharin
preference in 30 mouse strains. J Neurosci 2004;24:938–46. [PubMed: 14749438]
14. Max M, Shanker YG, Huang L, Rong M, Liu Z, Campagne F, Weinstein H, Damak S, Margolskee
RF. Tas1r3, encoding a new candidate taste receptor, is allelic to the sweet responsiveness locus
Sac. Nat Genet 2001;28:58–63. [PubMed: 11326277]
15. Li X, Li W, Wang H, Cao J, Maehashi K, Huang L, Bachmanov AA, Reed DR, Legrand-Defretin V,
et al. Pseudogenization of a sweet-receptor gene accounts for cats’ indifference toward sugar. PLoS
Genet 2005;1:27–35. [PubMed: 16103917]
16. Rajavel KS, Neufeld EF. Nonsense-mediated decay of human HEXA mRNA. Mol Cell Biol
2001;21:5512–9. [PubMed: 11463833]
17. Ferrell F. Preference for sugars and nonnutritive sweeteners in young beagles. Neurosci Biobehav
Rev 1984;8:199–203. [PubMed: 6205334]
18. Grace J, Russek M. The influence of previous experience on the taste behavior of dogs toward sucrose
and saccharin. Physiol Behav 1968;4:553–8.
19. Houpt KA, Coren B, Hintz HF, Hilderbrant JE. Effect of sex and reproductive status on sucrose
preference, food intake, and body weight of dogs. J Am Vet Med Assoc 1979;174:1083–5. [PubMed:
571424]
Li et al. Page 4
J Nutr. Author manuscript; available in PMC 2007 November 5.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
20. Houpt KA, Smith SL. Taste preferences and their relation to obesity in dogs and cats. Can Vet J
1981;22:77–85. [PubMed: 7248879]
21. Anderson B, Landgren A, Olsson L, Zotterman Y. The sweet taste fibers of the dog. Acta Physiol
Scand 1950;21:105–19. [PubMed: 14856761]
22. Kim U, Jorgenson ECH, Leppert M, Risch N, Drayna D. Positional cloning of the human quantitative
trait locus underlying taste sensitivity to phenylthiocarbamide. Science 2003;299:1221–5. [PubMed:
12595690]
23. Li X, Inoue M, Reed DR, Huque T, Puchalski RB, Tordoff MG, Ninomiya Y, Beauchamp GK,
Bachmanov AA. High-resolution genetic mapping of the saccharin preference locus (Sac) and the
putative sweet taste receptor (T1R1) gene (Gpr70) to mouse distal Chromosome 4. Mamm Genome
2001;12:13–6. [PubMed: 11178737]
24. Li X, Bachmanov AA, Li S, Chen Z, Tordoff MG, Beauchamp GK, de Jong PJ, Wu C, Chen L, et al.
Genetic, physical and comparative map of the subtelomeric region of mouse chromosome 4. Mamm
Genome 2002;13:5–19. [PubMed: 11773963]
25. Nelson G, Hoon MA, Chandrashekar J, Zhang Y, Ryba NJ, Zuker CS. Mammalian sweet taste
receptors. Cell 2001;106:381–90. [PubMed: 11509186]
26. Lu K, McDaniel AH, Tordoff MG, Li X, Beauchamp GK, Bachmanov AA, VanderWeele DA,
Chapman CD, Dess NK, et al. No relationship between sequence variation in protein coding regions
of the Tas1r3 gene and saccharin preference in rats. Chem Senses 2005;30:231–40. [PubMed:
15741599]
27. Gilad Y, Man O, Paabo S, Lancet D. Human specific loss of olfactory receptor genes. Proc Natl Acad
Sci U S A 2003;100:3324–7. [PubMed: 12612342]
28. Young JM, Friedman C, Williams EM, Ross JA, Tonnes-Priddy L, Trask BJ. Different evolutionary
processes shaped the mouse and human olfactory receptor gene families. Hum Mol Genet
2002;11:535–46. [PubMed: 11875048]
29. Gilad Y, Wiebe V, Przeworski M, Lancet D, Paabo S. Loss of olfactory receptor genes coincides with
the acquisition of full trichromatic vision in primates. PLoS Biol 2004;2:E5. [PubMed: 14737185]
Epub
30. Parry CM, Erkner A, le Coutre J. Divergence of T2R chemosensory receptor families in humans,
bonobos, and chimpanzees. Proc Natl Acad Sci U S A 2004;101:14830–4. [PubMed: 15466715]
Li et al. Page 5
J Nutr. Author manuscript; available in PMC 2007 November 5.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
FIGURE 1.
Gene structures of cat Tas1r3 and dog Tas1r3 (A), and cat Tas1r2 and dog Tas1r2 (B). The
exons are shown in black (size in bp). Location (bp) refers to the position within each exon.
Intron sizes shown in the figure are not proportionally scaled in (A) or (B) because of the large
size of the Tas1r2 introns. Under each dog exon is the percentage of similarity between that
exon and its cat counterpart at the nucleotide level (B). The exons for cat Tas1r2 refer to parts
corresponding to dog exons. Asterisks indicate the position of microdeletion in exon 3 as well
as the stop codon positions in exons 4 and 6 of cat Tas1r2. The accession for dog Tas1r3 is
AY916759, and for dog Tas1r2 is AY916758.
Li et al. Page 6
J Nutr. Author manuscript; available in PMC 2007 November 5.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
... Even though human panelists may evaluate sensory aspects (esp., appearance and aroma) of the pet food products and provide proportionate information about them, the results from pets and human panelists may differ mainly because pets (cats and dogs) and pet caregivers (humans) perceive aromas and flavors differently. For example, in contrast to humans, cats cannot perceive sweet taste because they lack a receptor for recognizing this taste (Baldwin et al., 2014;Li et al., 2006), while dogs can perceive the five taste qualities (Spence, 2022). As a result of these differences, researchers have developed methods to determine the acceptability and preferences of pet foods by employing pets as their panelists (Di Donfrancesco et al., 2012K.Koppel, 2014;Tobie et al., 2015). ...
Article
Full-text available
The pet food industry is a growing business launching a variety of new products in the market. The acceptability or preference of pet food samples has traditionally been measured using either one‐bowl or two‐bowl tests. Academic researchers and professionals in the pet food industry have explored other methods, including the cognitive palatability assessment protocols and the ranking test, to evaluate more than two samples. A variety of approaches and perspectives were also utilized to predict palatability and key sensory attributes of pet foods, including descriptive sensory analysis by human‐trained panelists and pet food caregivers’ perceptions of pet food. This review article examined a range of testing methods for evaluating the palatability of pet foods, specifically targeting products for dogs and/or cats. It outlined the advantages and disadvantages of each method. Additionally, the review provided in‐depth insights into the key sensory attributes of pet foods and the methodologies for assessing palatability. It also explored pets’ behavioral responses and facial expressions in relation to different pet foods. Furthermore, this review discussed current challenges and future opportunities in pet food development, including the use of instrumental analyses and artificial intelligence–based approaches.
... By contrast, medium-chain fatty acids, present in either the free form (e.g., 0.1% caprylic acid) or TAG (e.g., 5% medium-chain TAG), and 25% hydrogenated coconut oil in diets can reduce food intake by cats (MacDonald et al. 1985). Of particular note, cats cannot taste sweetness as indicated previously, because of the lack of sweet taste receptors due to the deletion of the Tas1r gene and, unlike dogs, do not select sweet substances such as sucrose (Li et al. 2005(Li et al. , 2006. For this reason, cats show no preference for sugar-rich foods such as fruits and juice. ...
Article
Full-text available
Domestic dogsand cats have evolved differentially in some aspects of nutrition, metabolism, chemical sensing, and feedingbehavior. The dogs have adapted to omnivorous dietscontaining taurine-abundant meat and starch-rich plant ingredients. By contrast, domestic catsmust consumeanimal-sourced foodsfor survival, growth, and development. Both dogsand catssynthesize vitamin C and many amino acids (AAs, such as alanine, asparagine, aspartate, glutamate, glutamine, glycine, proline, and serine), but have a limited ability to form de novo arginineand vitamin D 3 . Compared with dogs, cats have greater endogenousnitrogen losses and higher dietary requirements for AAs (particularly arginine, taurine, and tyrosine), B-complex vitamins (niacin, thiamin, folate, and biotin), and choline; exhibit greater rates of gluconeogenesis; are less sensitive to AA imbalances and antagonism; are more capable of concentrating urine through renal reabsorption of water; and cannot tolerate high levels of dietary starch due to limited pancreatic α-amylase activity. In addition, dogs can form sufficient taurinefrom cysteine(for most breeds); arachidonic acidfrom linoleic acid; eicosapentaenoic acid and docosahexaenoic acid from α-linolenic acid; all- trans- retinol from β-carotene; and niacinfrom tryptophan. These synthetic pathways, however, are either absent or limited in all cats due to (a) no or low activities of key enzymes (including pyrroline-5-carboxylate synthase, cysteinedioxygenase, ∆ ⁶ -desaturase, β-carotene dioxygenase, and quinolinate phosphoribosyltransferase) and (b) diversion of intermediates to other metabolic pathways. Dogs can thrive on one large meal daily, select high-fat over low-fat diets, and consume sweet substances. By contrast, cats eat more frequently during light and dark periods, select high-protein over low-protein diets, refuse dryfood, enjoy a consistent diet, and cannot taste sweetness. This knowledge guides the feeding and care of dogsand cats, as well as the manufacturing of their foods. As abundant sources of essentialnutrients, animal-derivedfoodstuffs play important roles in optimizing the growth, development, and health of the companionanimals.
Article
From a cognitive linguistic perspective, this article delves into the polysemy between the English term sour and its Chinese counterpart suan . The research aims to achieve two key objectives: (1) To explore the similarities and differences in the polysemy of sour in English and suan in Chinese. (2) To identify the cognitive mechanisms that motivate the semantic expansion of sour in English and suan in Chinese. To this end, 《汉语大词典》 (the Great Chinese Dictionary), The Oxford English Dictionary (OED), the British National Corpus (BNC), and the Centre for Chinese Linguistics (CCL) Chinese-English Parallel Corpus were used. The dictionaries are utilized to explore the polysemy of sour and suan , while the BNC and CCL Chinese-English Parallel Corpus are employed to investigate the cognitive mechanisms underlying the semantic extensions of the selected terms. Theoretically, this article draws upon the conceptual metaphor and metonymy theory proposed by Lakoff and Johnson. The findings reveal significant semantic overlap between sour in English and suan in Chinese, yet notable distinctions remain. This study has implications for vocabulary teaching as well as cross-linguistic and cross-cultural communication.
Article
Full-text available
Research into cognition in cats and the impact of nutrition on cat cognitive health lags behind that in dogs but is receiving increased attention. In this review, we discuss the evolutionary history of the domesticated cat, describe possible drivers of domestication, and explore the interrelationships between nutrition and cat cognition. While most cat species are solitary, domesticated cats can live in social groups, engage in complex social encounters, and form strong attachments to humans. Researchers have recently started to study cat cognition using similar methods as those developed for dogs, with an initial primary focus on perception and social cognition. Similar to dogs, cats also show cognitive and behavioral changes associated with stress and aging, but these signs are often gradual and often considered a consequence of natural aging. Despite the fundamental role of nutrition in cognitive development, function, and maintenance, research into the association between nutrition and cognition in cats is only preliminary. Ultimately, additional research is needed to gain a full understanding of cat cognition and to explore the role of nutrition in the cognitive health of cats to help improve their welfare.
Article
Full-text available
As for other mammals, the digestive system of dogs (facultative carnivores) and cats (obligate carnivores) includes the mouth, teeth, tongue, pharynx, esophagus, stomach, small intestine, large intestine, and accessory digestive organs (salivary glands, pancreas, liver, and gallbladder). These carnivores have a relatively shorter digestive tract but longer canine teeth, a tighter digitation of molars, and a greater stomach volume than omnivorous mammals such as humans and pigs. Both dogs and cats have no detectable or a very low activity of salivary α-amylase but dogs, unlike cats, possess a relatively high activity of pancreatic α-amylase. Thus, cats select low-starch foods but dogs can consume high-starch diets. In contrast to many mammals, the vitamin B12 (cobalamin)-binding intrinsic factor for the digestion and absorption of vitamin B12 is produced in: (a) dogs primarily by pancreatic ductal cells and to a lesser extent the gastric mucosa; and (b) cats exclusively by the pancreatic tissue. Amino acids (glutamate, glutamine, and aspartate) are the main metabolic fuels in enterocytes of the foregut. The primary function of the small intestine is to digest and absorb dietary nutrients, and its secondary function is to regulate the entry of dietary nutrients into the blood circulation, separate the external from the internal milieu, and perform immune surveillance. The major function of the large intestine is to ferment undigested food (particularly fiber and protein) and to absorb water, short-chain fatty acids (serving as major metabolic fuels for epithelial cells of the large intestine), as well as vitamins. The fermentation products, water, sloughed cells, digestive secretions, and microbes form feces and then pass into the rectum for excretion via the anal canal. The microflora influences colonic absorption and cell metabolism, as well as feces quality. The digestive tract is essential for the health, survival, growth, and development of dogs and cats.
Article
Full-text available
The ability to taste the sweetness of carbohydrate-rich foodstuffs has a critical role in the nutritional status of humans. Although several components of bitter transduction pathways have been identified1-6, the receptors and other sweet transduction elements remain unknown. The Sac locus in mouse, mapped to the distal end of chromosome 4 (refs. 7-9), is the major determinant of differences between sweet-sensitive and -insensitive strains of mice in their responsiveness to saccharin, sucrose and other sweeteners10-13. To identify the human Sac locus, we searched for candidate genes within a region of approximately one million base pairs of the sequenced human genome syntenous to the region of Sac in mouse. From this search, we identified a likely candidate: T1R3, a previously unknown G protein-coupled receptor (GPCR) and the only GPCR in this region. Mouse Tas1r3 (encoding T1r3) maps to within 20,000 bp of the marker closest to Sac (ref. 9) and, like human TAS1R3, is expressed selectively in taste receptor cells. By comparing the sequence of Tas1r3 from several independently derived strains of mice, we identified a specific polymorphism that assorts between taster and non-taster strains. According to models of its structure, T1r3 from non-tasters is predicted to have an extra amino-terminal glycosylation site that, if used, would interfere with dimerization.
Article
Full-text available
We report a comprehensive comparative analysis of human and mouse olfactory receptor (OR) genes. The OR family is the largest mammalian gene family known. We identify ∼93% of an estimated 1500 mouse ORs, exceeding previous estimates and the number of human ORs by 50%. Only 20% are pseudogenes, giving a functional OR repertoire in mice that is three times larger than that of human. The proteins encoded by intact human ORs are less highly conserved than those of mouse, in patterns that suggest that even some apparently intact human OR genes may encode non-functional proteins. Mouse ORs are clustered in 46 genomic locations, compared to a much more dispersed pattern in human. We find orthologous clusters at syntenic human locations for most mouse genes, indicating that most OR gene clusters predate primate–rodent divergence. However, many recent local OR duplications in both genomes obscure one-to-one orthologous relationships, thereby complicating cross-species inferences about OR–ligand interactions. Local duplications are the major force shaping the gene family. Recent interchromosomal duplications of ORs have also occurred, but much more frequently in human than in mouse. In addition to clarifying the evolutionary forces shaping this gene family, our study provides the basis for functional studies of the transcriptional regulation and ligand-binding capabilities of the OR gene family.
Article
Full-text available
Differences in sweetener intake among inbred strains of mice are partially determined by allelic variation of the saccharin preference (Sac) locus. Genetic and physical mapping limited a critical genomic interval containing Sac to a 194 kb DNA fragment. Sequencing and annotation of this region identified a gene (Tas1r3) encoding the third member of the T1R family of putative taste receptors, T1R3. Introgression by serial backcrossing of the 194 kb chromosomal fragment containing the Tas1r3 allele from the high-sweetener-preferring C57BL/6ByJ strain onto the genetic background of the low-sweetener-preferring 129P3/J strain rescued its low-sweetener-preference phenotype. Polymorphisms of Tas1r3 that are likely to have functional significance were identified using analysis of genomic sequences and sweetener-preference phenotypes of genealogically distant mouse strains. Tas1r3 has two common haplotypes, consisting of six single nucleotide polymorphisms: one haplotype was found in mouse strains with elevated sweetener preference and the other in strains relatively indifferent to sweeteners. This study provides compelling evidence that Tas1r3 is equivalent to the Sac locus and that the T1R3 receptor responds to sweeteners.
Article
Full-text available
Conducted 4 experiments with 28 domestic and 12 wild cats to examine flavor preference in cats. In the 1st experiment domestic Ss exhibited no preference (both in 24-hr and 1-hr 2-choice preference tests) for any of a variety of carbohydrate or artificial sweeteners regardless of whether a water or saline diluent was employed. A preference for sucrose or lactose dissolved in dilute milk compared with dilute milk alone was observed. This preference may have been based on textural rather than flavor characteristics of the milk-sugar solution. In the 2nd experiment a similar lack of preference for carbohydrate sweeteners was found when using 5-min 2-choice preference tests with wild Ss (genus Panthera). In light of this lack of sweet preference among cats, Exps III and IV examined responses to solutions of hydrolyzed protein and individual amino acids and to emulsified fat mixtures. Solutions of hydrolyzed soy, lactalbumin, and casein; l-alanine and l-proline solutions; and butterfat mixtures were all preferred to the diluent. It is suggested that a pattern of responses characterized by an avidity for protein and fat products and no avidity for carbohydrate sweeteners may be typical of strict carnivores like cats. (21 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Article
Full-text available
The Sac (saccharin preference) locus affecting mouse behavioral and neural responsiveness to sweeteners has been mapped to distal Chr 4. A putative sweet taste receptor, T1R1, has been recently cloned, and the gene encoding it, Gpr70, has also been mapped to mouse distal Chr 4. To assess Gpr70 as a candidate gene for Sac, we compared the Gpr70 sequences of C57BL/6ByJ and 129P3/J mouse strains with different alleles of Sac. Using Gpr70 sequence variation between the C57BL/6ByJ and 129P3/J strains, we conducted a high-resolution analysis of the chromosomal localization of the Gpr70 and Sac loci in the F2 hybrids and 129.B6-Sac partially congenic mice originating from these two strains. The Gpr70 gene maps proximal to Sac, which demonstrates that they are different loci.
Article
A study of the influence of congenital factors and past experience on taste preference for several aqueous solutions was carried out on 13 newborn puppies and 20 adult dogs. The adult dogs showed a strong rejection of saccharin (0.1%) and quinine (0.01%), a mild rejection of saline (0.9%), and a strong preference for sucrose (10%). Since pups showed the same rank order of preferences for these solutions, the preferences appear to be congenital. Nevertheless, the preference of adult dogs for sucrose (relative to water) could be transformed into a rejection after imposition of four days of continuous access to water and saccharin solution; this conditioned rejection was extinguished with repeated exposure during the next few days. Conversely, the rejection of saccharin was sometimes replaced by preference during the first day that followed several days of experience with water and sucrose; this again was extinguished rapidly. In some cases, when saccharin followed a previous experience with sucrose, the dogs exhibited characteristics of experimental neurosis (in the Pavlovian sense); that is, they reduced intake of both water and saccharin, showing a decrease of total fluid intake of more than 85%.
Article
Six naturally occurring compounds which have been observed to be physiologically active in the anesthetized cat were demonstrated to be behaviorally active in terms of preference and avoidance in 11 cats. Using a 2-bottle long-term preference experiment, concentrations of .5, 5, 50 mM levoproline, levolysine, levohistidine, levotryptophan, levoisoleucine, and adenine (all in 50 mM NaCl) were compared against 50 mM saline. At 50 mM concentration, those chemicals which elicit an increase in spike output from geniculate ganglion chemoresponsive group II units (levoproline, levolysine, and levohistidine) were preferred, while levotryptophan, levoisoleucine, and adenine, which decrease group II discharge, were avoided. The preference response to levoproline was then observed over a concentration range extending to 500 mM. Maximum response was observed at 50 mM, with preference decreasing as concentration was either increased or decreased. (43 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Article
Thesis (Ph. D.)--University of California, Los Angeles, 2001. Typescript (photocopy). Vita. Includes bibliographical references.