Fat Taste

Traditionally, fat in foods was thought to be perceived through textural cues, such as creaminess and oiliness. The thought that fat might have a detectable taste was only recognized in the past few years, first in animal studies, and then more recently in humans. Previous literature identified only five basic taste sensations: sweet, sour, bitter, salty, and umami (L–amino acid). However, recent studies point to the possibility of a receptor system for fat, hence a fat taste. Dietary fat was thought to be perceived exclusively by trigeminal (textural) and olfactory cues, but it seems that taste plays an important role in fat sensing as well. Fat taste may be one mechanism that has developed to promote increased consumption of the nutrient. This could lead to health problems, since preference for high-fat foods and excessive fat intake in humans increases risk for numerous diseases, such as obesity, diabetes, heart disease, hypertension, and cancer.

Taste perception occurs when molecules of food or drink contact and activate taste cells, which are assembled into buds and located at various sites, such as the tongue, throat, and upper esophagus. Fats or their constituents may stimulate some or all of these buds. Although most dietary fat consists of triacylglycerol (TAG), long-chain fatty acids (LCFAs), which are released from TAG by the enzyme lingual lipase, allow for some free fatty acids to be liberated in the oral cavity where they can activate taste cells. In fact, when lingual lipase is blocked, rodents show a considerable reduction in there fat preferences, presumably because the ability to taste fats has been blocked.

One protein that has been implicated as a potential fat taste receptor is CD36, also known as FAT for fatty acid translocase. CD36 is expressed in human and rodent taste papillae, as well as a variety of other tissues, and it functions to transport long chain fatty acids (LCFA) across the cell membrane. Once LCFAs are delivered inside the [Page 267]cell, they are able to transmit information about fat taste stimuli to the brain. When rodents were made CD36-deficient, the high palatability of LCFA-enriched solutions was completely abolished, so in a sense, the absence of CD36 made these animals unable to form fat preferences. This finding has yet to be replicated in humans.

Fatty acid taste may involve more than the oral cavity. Research suggests that fat is tasted in postoral regions of the gastrointestinal tract, such as the intestine, and other areas of the body, such as adipose tissue, skeletal muscle, heart, and brain. The expression fat taste is used to define the detection of fatty acids even beyond the oral cavity because the CD36 taste transduction mechanism seems to be universal and apply to the other fat-sensing tissues besides the GI tract.

Fat taste may activate the metabolic response to dietary fat. In humans and animals, sham studies following oil capsule ingestion demonstrated that oral fat exposure stimulated larger postprandial elevations in circulating TAG than exposure to nonfat stimuli or no oral stimulation. Follow-up studies revealed that the taste component, and not the olfactory stimulation, from the oral exposure of fat was the metabolic cue for the rise in circulating TAG.

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