Abstract: Taste is the chemical sense responsible for the detection of non-volatile chemicals in potential foods. For fat to be considered as one of the taste primaries in humans, certain criteria must be met including class of affective stimuli, receptors specific for the class of stimuli on taste bud cells (TBC), afferent fibres from TBC to taste-processing regions of the brain, perception independent of other taste qualities and downstream physiological effects. The breakdown products of the macronutrients carbohydrates (sugars) and proteins (amino acids) are responsible for the activation of sweet and umami tastes, respectively. Following the same logic, the breakdown products of fat being fatty acids are the likely class of stimuli for fat taste. Indeed, psychophysical studies have confirmed that fatty acids of varying chain length and saturation are orally detectable by humans. The most likely fatty acid receptor candidates located on TBC are CD36 and G protein-coupled receptor 120. Once the receptors are activated by fatty acids, a series of transduction events occurs causing the release of neurotransmitters towards afferent fibres signalling the brain. Whether fatty acids elicit any direct perception independent of other taste qualities is still open to debate with only poorly defined perceptions for fatty acids reported. Others suggest that the fatty acid taste component is at detection threshold only and any perceptions are associated with either aroma or chemesthesis. It has also been established that oral exposure to fat via sham feeding stimulates increases in blood TAG concentrations in humans. Therefore, overall, with the exception of an independent perception, there is consistent emerging evidence that fat is the sixth taste primary. The implications of fatty acid taste go further into health and obesity research, with the gustatory detection of fats and their contributions to energy and fat intake receiving increasing attention. There appears to be a coordinated bodily response to fatty acids throughout the alimentary canal; those who are insensitive orally are also insensitive in the gastrointestinal tract and overconsume fatty food and energy. The likely mechanism linking fatty acid taste insensitivity with overweight and obesity is development of satiety after consumption of fatty foods.
Alex’s Notes: Taste is an interesting aspect of our evolutionary and sociocultural upbringings. On the one hand, we perceive taste to be a combination of sweet, sour, salty, bitter, and umami in order to inform us about the potential nutrition and/or toxins contained within the food. On the other hand, taste is a learned preference that may change over a lifetime. Regardless, given the evolutionary purpose of taste, it stands to reason that fats should be detected as a dense source of energy, just as carbohydrates (sweet) and protein (umami) are.
And while fat has indeed been classified as a taste since the times of Aristotle, modern science demands that it meet five criteria:
- There must be a distinct class of affective stimuli.
The distinctive stimuli for fat are, unsurprisingly, fatty acids. Since dietary fat is almost entirely consumed in the form of triglycerides, there needs to be a method for freeing the fatty acids from the glycerol backbone within the mouth. This is job belongs to lingual lipase. However, although this enzyme is a main player in the infant’s digestive process, its role in adults is less clear and it is not known if we maintain the ability to produce it or rely on oral microbes.
- There should be transduction mechanisms including receptors to change the chemical code of the stimuli to electrical signal.
The most likely receptor within taste bud cells (TBC) to react to fatty acid stimulation is CD36, which for what it’s worth, just happens to be an integral membrane protein of nearly all cells in body that works to uptake free fatty acids from circulation. It is also a main transporter of fat from the lumen into intestinal cells. In addition, G protein-coupled receptor 120 (GPCR120) has been suggested to be involved in a signaling cascade to detect fatty acids.
- There must be neurotransmission of the electrical signal to processing regions of the brain.
Unfortunately, this area of research is lacking. It has been shown that the neurotransmitters noradrenaline and serotonin are secreted towards afferent nerve fibers which trigger the orosensory perception, but further work is necessary to figure out the specifics of fat taste transmission.
- There should be perceptual independence from other taste qualities.
For every taste there exists a continuum. At low concentrations, certain food components such as fatty acids may be detected, but cannot be recognized as a taste. As concentration increases, so does our ability to recognize the taste. If the concentration becomes too great, then we crossed over into gross-land where the flavor is general unpleasant. It seems counter-intuitive to think that whether there is a recognizable taste quality associated with fat is still up for debate, but consider our abilities to taste sweet or salty foods; a lot easier and more identifiable than fat right?
- Finally, there must be physiological effects after activation of taste bud cells.
Simply tasting fat prepares the body for fat digestion and absorption, with a 2.8-fold increase in plasma triglyceride concentrations. Moreover, these effects are not observed in fat-mimics with similar sensory characteristics. There also appears to be a transient increase in gastric lipase secretion, cholecystokinin (CCK), pancreatic polypeptide (PP) and peptide YY (PYY).
Fat as the sixth taste has yet to be determined. However, as evidence continues to accumulate, it may indeed become one in the next five to ten years.
The real question here is, why does this matter? The answer is based on rough logic, but essentially, fat is the most energy dense nutrient and a preference for fat taste may influence fat consumption and potentially weight status. As we know, weight regulation is more complex than eat fat get fat. Nonetheless, a unique feature of the taste system is the huge inter-individual differences, and differences in dietary preferences between lean and obese persons are well established.
Studies in twins have shown that acquired preference for fatty foods is associated with obesity, independent of genetic background. It has also been found that those who are more sensitive to oleic acid (18:1; the main fatty acid of monounsaturated fats such as olive oil) have lower energy intake, fat consumption, and BMI. These “hypersensitive” people are more likely to trim the excess fat off their meat and limit saturated fats. Conversely, “hyposensitive” people consumed more high-fat dairy, high-fat spreads, and high-fat meats. They also had greater BMIs.
These fat preferences may also create a cycle that is best known in people who overconsume sugars or do drugs whereby more is needed to generate stimulation. Many people ignorantly call sugar a drug; well perhaps we should start saying that for fat as well. In both obese and lean individuals, a low-fat diet increases sensitivity and reduces preference for fat. However, a high-fat diet decreases taste sensitivity to fat only in lean persons, suggesting that obese people may be adapted to high-fat exposure.
In normal weight persons, fat in the gut produces potent satiety signals such as CCK, PYY, and ghrelin. These physiological signals may be impaired in obesity, with consumption of fatty foods being voluntarily twice as great when compared to normal weight controls.
So fat may not yet be a taste, per se, but it does play a role in obesity. It appears that obese individuals are less sensitive to the sensory properties of fat and also suffer from blunted physiological responses. What has yet to be determined is whether the obesity led to a lack of taste, or if the lack of taste led to obesity.