Trait#99: Fat taste sensitivity (CD36)
Monday, June 07, 2021. Author FitnessGenes
Monday, June 07, 2021. Author FitnessGenes
As omnivores capable of ingesting a wide variety of foods, our ancient ancestors required a way of detecting which foods were nutritious, and which were potentially poisonous. Similarly, we needed a way of preparing the gut to digest and assimilate the nutrients about to be received.
It’s thought that we evolved taste perception to solve these adaptive problems. In this respect, humans have evolved five basic tastes (known as taste primaries) – sweet, sour, salty, bitter and umami (savory taste). These taste primaries allow us to perceive desirable nutrients (at the appropriate quantities) as pleasant, but perceive potential toxins (at harmful levels) as unpleasant.
For example, sugar, a rich source of energy, produces a pleasant, sweet sensation. By contrast, ricin, a toxin found in castor beans that can cause blood clots, tastes unpleasantly bitter.
Given the importance of fat as nutrient, which is needed for making cell membranes, protecting organs, creating energy stores, and producing hormones, it is not completely surprising that we have also evolved mechanisms for tasting fat.
If you’ve ever looked at or touched the surface of your tongue, you’ll have noticed it’s covered in small, nipple-like projections that give it a rough texture. These projections are called papillae, which are, in turn, covered in taste buds.
Taste buds house collections of specialized cells called taste receptor cells. These cells have receptors that become activated and generate electrical impulses in response to certain nutrients in food (called tastants).
Different classes of taste receptor cells, which are located in different regions of the tongue, are responsible for the five different taste primaries: sweet, sour, salty, bitter and umami. As we’ll explore in this article, we also have taste receptors (e.g. CD36) that are activated by fats in our food.
Once stimulated, taste receptors generate electrical impulses that convey information about taste, which is then transmitted along sensory nerves (specifically, the facial, glossopharyngeal, and vagus nerves) to a region of the brain called the medulla oblongata.
From the medulla, taste information is relayed to higher areas in the brain, namely the gustatory cortex, which gives rise to the sensation of taste.
Taste information is also relayed to the digestive tract, which allows the digestive system to prepare itself (e.g. by secreting enzymes, priming bowel movement) for the receipt of food.
High-fat foods, such as fatty meats, cakes, fried foods, and full-fat dairy products, are highly palatable and give us a pleasurable sensation when we eat them. This is partly due to their texture, smell, and stimulation of the five taste primaries (e.g. fatty meats are often high in salt, switch stimulates salt taste; cakes and chocolate are rich in sugar, which stimulates sweet taste).
Studies where these factors (e.g. texture, smell, sugar content) are masked or controlled for, however, suggest that we are also directly sensitive to the presence of fat in our food.
In addition to the five taste primaries (sweet, salt, sour, bitter, and umami), it is shown that our tongues can also chemically detect fat or, more specifically, fatty acids – the building blocks of fat.
Source: Gaillard, D., & Kinnamon, S. C. (2019). New evidence for fat as a primary taste quality. Acta physiologica (Oxford, England), 226(1), e13246.
Whenever we eat foods that contain fat, some of the fat is broken down in our mouth, yielding fatty acids. These fatty acids then stimulate specialized fat taste receptors on our tongue, which convey information about the presence of fats via sensory nerves to our brain and digestive system.
In response, the digestive system can prime itself to break down fats by secreting fat-digesting enzymes. It also secretes satiety hormones that make us feel full and limit excess food intake.
It is still a matter of debate as to whether stimulation of fat taste receptors gives rise to the perceptual taste of fat, in the same way sugar gives rise to a sweet-tasting sensation. It may be the case that our tongues are chemically sensitive to fatty acids, but that fatty acids in the mouth do not generate a distinct ‘taste’ of fat.
It’s tempting to think that the process of chemically digesting food begins in the stomach, but we actually secrete enzymes that partially digest food in our mouth. For example, our saliva contains an enzyme called salivary amylase, which helps break down starch into smaller sugar molecules.
In a similar fashion, we also secrete an enzyme called lingual lipase into our saliva, which helps break down fats (in the form of triglycerides) into smaller fatty acid molecules.
Once fatty acids are formed in the mouth, they bind to and activate various fat/ fatty acid taste receptors on the surface of our tongue. It is thought that there are several different kinds of fat taste receptors, which are sensitive to fatty acids of different sizes/ lengths.
One type of fat taste receptor, known as CD36 (cluster of differentiation 36) is particularly sensitive to long chain fatty acids. When these bind to the CD36 receptor, they trigger a signalling cascade, which results in an electrical impulse that is transmitted along nerve fibres to the brain and digestive system.
Source: Abumrad, N. A. (2005). CD36 may determine our desire for dietary fats. The Journal of clinical investigation, 115(11), 2965-2967.
As mentioned earlier, the nerve fibres transmit taste information to higher parts of the brain, including the gustatory cortex, which alert the body that we are consuming fat. Information is also relayed to the digestive system, which primes the gut to digest fat.
In this respect, when fatty acids bind to and stimulate CD36 receptors in the tongue, it triggers feed-forward mechanisms that cause the gut and pancreas to secrete enzymes (e.g. lipases) that break down fat.
Furthermore, it causes the pre-emptive release of satiety hormones, such as cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), and peptide YY (PYY), which give rise to feelings of fullness and prevent excessive food intake. Similarly, activation of CD36 receptors also inhibits the secretion of the ‘hunger hormone’ ghrelin.
In this way, CD36 receptors (as well as other fatty acid taste receptors) not only allow us to detect the presence of fatty acids in the mouth but, by altering gut satiety, regulate how much fat we consume.
Changes in the function of CD36 receptors and our ability to detect fatty acids in the mouth can therefore influence our fat intake. More specifically, impaired function of CD36 receptors would be expected to lead to lower sensitivity to fatty acids and, consequently, reduced gut satiety and a higher fat intake.
The CD36 fat taste receptor is encoded by the CD36 gene.
Studies suggest that variants of this gene can affect fatty acid taste sensitivity. On this note, a SNP (Single Nucleotide Polymorphism) within the CD36 gene, designated rs1761667, generates two different CD36 gene variants or alleles: ‘A’ and ‘G’.
Of these variants, the ‘A’ allele has been linked to reduced fat taste sensitivity.
But, what exactly do we mean by reduced fat taste sensitivity?
Experiments on fat taste sensitivity usually involve getting subjects to taste solutions that contain gradually increasing concentrations of fatty acids (e.g. oleic acid).
Subjects then report when they can first detect the presence of something in the solution that isn’t water. The concentration of fatty acid present in the solution at this point is known as the detection threshold.
A higher than average detection threshold (i.e. a larger concentration of fatty acid required in the solution in order to be detected) corresponds to lower fat taste sensitivity.
Various studies have shown that the ‘A’-allele is linked to a higher fatty acid detection threshold and lower fat taste sensitivity. For example, one study found that people with two copies of the ‘A’ allele (AA genotype) had a significantly higher detection threshold for oleic acid (a long-chain fatty acid).
As shown in the graph below, the ‘A’ allele (rs1761667) had an ‘additive effect’ on fat taste sensitivity. While not as low as in those with two copies (AA genotype), individuals with one copy of the ‘A’ allele (i.e. the GA genotype) had lower fat taste sensitivity compared to those with the GG genotype.
Melis, M., Sollai, G., Muroni, P., Crnjar, R., & Tomassini Barbarossa, I. (2015). Associations between orosensory perception of oleic acid, the common single nucleotide polymorphisms (rs1761667 and rs1527483) in the CD36 gene, and 6-n-propylthiouracil (PROP) tasting. Nutrients, 7(3), 2068-2084.
So, why do ‘A’ allele carriers have reduced fat taste sensitivity?
It’s thought that the ‘A’ allele of the CD36 gene leads to lower expression of the CD36 receptor on taste receptor cells within taste buds. A lower amount of CD36 receptors on the surface of the tongue would then mean it is harder to detect a given amount of fatty acids in the mouth.
Furthermore, in compensation for reduced fat/fatty acid taste sensitivity, ‘A’ allele carriers may consume more fat in their diet. For example, in a cross-sectional study of Japanese subjects, those with the AA genotype consumed a significantly higher amount of total fat (median intake = 44.5 g/day) and monounsaturated fatty acids (MUFAs) compared to those with GA (41.7 g/day) and GG (42.5 g/day) genotypes.
Part of this increased fat intake linked to the ‘A’ allele may be due to an impaired satiety response to consuming fat. This would lead to 'A' allele carriers feeling less full after eating fat-containing foods.
On this note, one study found that ‘A’ allele carriers had lower levels of the satiety hormone peptide YY (PYY) compared to those with the GG genotype. This is illustrated in the graph below. (Interestingly, this effect of CD36 genotype on PYY levels was not present in subjects following a vegetarian diet, suggesting that diet can modify the effect of CD36 genes on gut satiety).
Source: Karthi, M., Deepankumar, S., Vinithra, P., Gowtham, S., Vasanth, K., Raj, P. P., ... & Selvakumar, S. (2021). Single nucleotide polymorphism in CD36: Correlation to peptide YY levels in obese and non-obese adults. Clinical Nutrition, 40(5), 2707-2715.
Reduced fat taste sensitivity, increased fat intake, and an impaired gut satiety response to consuming fat may also drive weight gain in ‘A’ allele carriers. Although findings are somewhat mixed, some studies have linked to the ‘A’ allele to higher BMI and an increased risk of obesity.
Your fat taste sensitivity isn’t just affected by what CD36 gene variants that you inherit. Lifestyle factors, such as your diet or current bodyweight, also strongly influence your ability to detect fatty acids in the mouth and initiate a satiety response in response to fat intake.
With regards to diet, studies suggest that high intakes of fats can worsen fat-taste sensitivity. For example, in one crossover trial, subjects had significantly elevated fatty acid detection thresholds (i.e. lower fat taste sensitivity) after consuming a high-fat diet over 4 weeks in which fat accounted for more than 45% of total calorie intake.
The reason for this is likely due to a process of receptor desensitisation – a well-known phenomenon in physiology. If someone consistently eats a high-fat diet, CD36 taste receptors on the surface of the tongue are constantly stimulated by fatty acid molecules. As a result, the body responds by reducing (or ‘downregulating’) the number of CD36 receptors expressed. This leads to lower fat taste sensitivity, as a greater amount of fatty acids is needed to stimulate the now lower number of CD36 receptors present on tongue. Similarly, a greater amount of fatty acids is needed to trigger a satiety response. In a vicious cycle, this then leads to greater fat intakes, which again worsens fat taste sensitivity.
It is thought that high dietary intakes of fat in the long-term is one reason why people who are overweight and obese are shown to have lower fat taste sensitivity.
Source: Newman, L. P., Bolhuis, D. P., Torres, S. J., & Keast, R. S. (2016). Dietary fat restriction increases fat taste sensitivity in people with obesity. Obesity, 24(2), 328-334.
The good news is that just as a high-fat diet can worsen fat taste sensitivity, studies suggest that a low-fat diet can increase expression of CD36 receptors and improve fat taste sensitivity. For example, in one study, overweight and obese subjects following a 6-week low-fat diet, in which less than 25% of total calories came from fat, developed lower fatty acid detection thresholds (i.e. increased fat taste sensitivity).
Again, the reason for this effect is likely due to receptor resensitisation, in which lower stimulation of CD36 receptors by fatty acids in the mouth leads to a compensatory increase in the number of CD36 receptors expressed on the tongue.
Greater fat taste sensitivity also means less fatty acids in the mouth are needed to initiate a satiety response, leading to less overall fat being consumed.
Your Fat taste sensitivity (CD36) trait looks at both CD36 gene variants (created by the rs1761667 SNP) and your lifestyle survey data to assess your taste sensitivity to fatty acids.
Your trait results will fall into one of four categories:
To find out your trait result, please log in to truefeed.
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