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.
The sense of taste
The sense of taste presumably evolved to inform us about the nutritious or toxic value of potential foods. The primary organ responsible for the sense of taste is the tongue, which contains the biological machinery (taste receptors) to identify non-volatile chemicals in foods and non-foods we place in our mouth. Once a food enters the mouth, the tongue aids in the manipulation of the food, assisting breakdown and bolus formation before swallowing the food. During this critical period of food manipulation, the tongue is sampling chemicals in the food, and when food chemicals activate taste receptors, signals are sent from the taste receptors to processing regions of the brain. The signals are decoded by the brain, and we perceive the taste of the food, which could be one of five distinct qualities: sweet, sour, salty, bitter and umami.
It is perhaps appropriate to classify taste as a nutrienttoxin detection system, with the qualities (sweet, etc.) informing us via an associated hedonic response of suitability to swallow or reject, for example sweet elicited by sugars reflecting carbohydrate, sour elicited by free hydrogen ions (H+ ) reflecting excessive acid, umami elicited by glutamate and other amino acids reflecting protein content, salt elicited by sodium (Na+ ) and other ions reflecting mineral content, and bitter reflecting potential toxins in foods. Excessive bitterness or sourness is aversive and informs that the food in our mouth may cause harm and that the best action is to expectorate, whereas the qualities sweet, umami and salty are all appetitive within a relevant intensity range and inform that the food contains compounds we should ingest, in this case, essential nutrients such as carbohydrate, protein and minerals, respectively. As the taste system has evolved to detect the nutrients or toxins in foods prior to ingestion, it makes sense that fats, an essential energy-dense macronutrient required in limited amounts for energy and nutritional needs, would be detected through taste, as other macronutrients namely carbohydrates and proteins are detected through the tastes of sweet and umami.
Fat taste is an area of increasing interest particularly in chemosensory and nutrition research with the possibility that it may be linked with dietary consumption of fatty foods. The intake and regulation of dietary fats is considered especially important in the development of overweight and obesity, given their high energy density and palatability alongside their ability to promote excess energy intake. The intake and regulation of fats in the obese state appears especially problematic given that obese persons prefer higher fat foods that represent significant portions of the obese diet.
Fat has been classified as a taste as early as 330 BC by Aristotle and many other academics over the centuries . More recently, fat has been associated with texture, flavour release and thermal properties in foods, but not the sense of taste . This may seem like an irrelevant academic point, but the taste system is only activated when a saliva-soluble component of a potential food activates receptors on taste cells. Adding to the importance of the sense of taste is the interplay between taste cell activation and multiple digestive processes, therefore making the link between taste and fat intake very important, especially given the link dietary fat has with the development of obesity.
For fat to be generally accepted as a taste, it must meet five criteria: 1) There must be a distinct class of affective stimuli, and the stimuli responsible for fat taste are the breakdown products of fats and fatty acids [3,4]. 2) There should be transduction mechanisms including receptors to change the chemical code of the stimuli to electrical signal. Emerging evidence suggests that CD36 and G protein-coupled receptor (GPCR) 120 are the most likely candidate receptors on taste bud cells (TBC), with multiple taste transduction mechanisms also involved . 3) There must be neurotransmission of the electrical signal to processing regions of the brain [6,7]. 4) There should be perceptual independence from other taste qualities. This criterion is controversial, and while there is certainly no obvious perception such as the sweetness of sucrose or saltiness of NaCl, some researchers claim less well-defined perceptions for fatty acids . Others suggest that the fatty acid taste component is at detection threshold only and any definable perceptions are associated with either aroma or chemesthesis [4,9]. 5) Finally, there must be physiological effects after activation of taste bud cells.
What follows is a brief summary of evidence supporting fat as the sixth taste and potential relevance of fat taste sensitivity to food consumption and development of obesity.
Fatty acids as stimuli
While it is well established that oxidised or reverted fatty acids or fatty acids at high concentrations are unpleasant to taste, the taste quality of fatty acids will vary according to their concentration in a food. The levels of fatty acids involved in fat taste are low enough not to be considered unpleasant in unspoiled food, yet sufficient to activate putative oral receptors. For example, the concentrations of fatty acids required for detection are within ranges which may be inherently present in edible fresh and processed foods (0.1%–3% w/v) , or perhaps made available through enzymatic hydrolysis by lingual lipase.
Lipase enzymes are very important as they break the triacylglycerols (TAGs) down so that free fatty acids can be transduced by cellular pathways. In humans, however, lingual lipase presence remains controversial. Data has suggested that lipolytic activity may be present in humans [9,11], although it is unknown whether sufficient concentrations of lingual lipase are produced and whether this originates from endogenous sources or oral microbes. The presence of lipase does appear to have an influence on fatty acid thresholds with research showing that the addition of orlistat (lipase inhibitor) during testing increased fatty acid thresholds . Overall, the weight of evidence suggests that free fatty acids in fatty foods will be in sufficient concentrations to activate putative receptors on taste cells.