In a 2015 review article, Russell S. J. Keast and Andrew
Costanzo argue that for fat to be considered a taste, it must
meet the following criteria: 1) There must be a distinct class of
chemicals that stimulate the fat taste; 2) there must be signal
transduction mechanisms to convert the chemical stimuli to
an electrical signal; 3) the electrical signal must be transmitted
by neurons to processing regions of the brain; 4) the fat taste
should be distinguishable from other tastes; and 5) there must
be physiological effects following activation of the taste bud
cells ( http://dx.doi.org/10.1186/2044-7248-4-5).
Let’s examine the evidence for each of these criteria:
1) There must be a distinct class of chemicals that stimulate the
Just as the breakdown products of carbohydrates (
sugars) and proteins (amino acids) are responsible for sweet and
umami tastes, respectively, the likely stimulus for fat taste is
fatty acids, the breakdown products of triglycerides. A lipase
enzyme in the saliva, called lingual lipase, cleaves a portion of
ingested triglycerides into free fatty acids (the remainder are
broken down further in the gastrointestinal tract). The released
free fatty acids can then bind to putative receptors on taste
bud cells to elicit downstream effects.
Humans can easily detect the unpleasant taste of oxidized
fatty acids, which are typically present at high concentrations
in spoiled food. However, the levels of fatty acids that stimulate fat taste are low enough to not be considered unpleasant,
but high enough to activate receptors on taste bud cells (Keast,
R. S. J., and Costanzo, A., http://dx.doi.org/10.1186/2044-7248-
4-5, 2015). In human taste tests, this level corresponded to
0.1%–3% w/v fatty acids inherent in fresh and processed foods
(not considering the free fatty acids potentially released by
2) There must be signal transduction mechanisms to convert
the chemical stimuli to an electrical signal.
The most convincing fat taste receptor identified so far is
the fatty acid transporter CD36, found on human taste buds
cells. Researchers have found that variations in the CD36 gene
influence fat sensitivity (Pepino, M. Y., et al., http://dx.doi.
org/10.1194/jlr.M021873, 2012). In a 2012 study, participants
were given three different cups of solutions, one of which
contained a small amount of a fatty oil. The other two cups
contained solutions similar in texture but fat-free. The
researchers asked the participants to choose the cup that was
different. The same three-cup test was repeated several times,
with different concentrations of fat. “If we had asked, ‘does it
taste like fat to you?’ that could be very subjective,” said first
author M. Yanina Pepino of Washington University School of
Medicine in St. Louis, Missouri, USA, in a news release. “So we
tried to objectively measure the lowest concentration of fat
at which someone could detect a difference.”
People who made the most CD36 were eight times more
sensitive to the presence of fat than those who made 50% less
of the protein. This study is consistent with animal experiments
in which rodents genetically engineered to lack functional
CD36 ceased to display a preference for fatty foods.
The CD36 receptor has an extracellular, hydrophobic
pocket that binds both saturated and unsaturated long-chain fatty acids (LCFA) with an affinity in the nanomolar
range (Besnard, P., et al., http://dx.doi.org/10.1152/phys-
rev.00002.2015, 2016). CD36 and associated LCFA have been
detected in lipid rafts—clusters of signaling molecules—in
the membranes of taste bud cells. Besnard and colleagues
proposed a model (supported by experimental data) in
which binding of LCFA to CD36 initiates a signaling cascade in
taste bud cells that results in calcium accumulation and cell
depolarization, an electrical signal that can be transmitted
to the brain. Although the evidence is less consistent, other
receptors have been proposed to sense or modulate the fat
taste. For example, the G protein-coupled receptor GPR120 on
taste bud cells binds to and is activated by fatty acids. However, mice lacking GPR120 still show a preference for fatty
foods, indicating that the receptor is not essential for fat taste
sensation. It is possible that GPR120 cooperates with CD36 to
modulate fat taste sensitivity (Besnard, P., et al., http://dx.doi.
Is fat really the sixth taste?
Olio is an Inform column that highlights research, issues, trends,
and technologies of interest to the oils and fats community.
The past year has been full of headlines about the elusive sixth taste: oleogustus, as some researchers
have termed it, or “the unique taste of fat” (Running, C. A., et al., http://dx.doi.org/10.1093/chemse/
bjv036, 2015). Recent studies and review articles have made the case that fat should join salty, sweet,
bitter, sour, and umami as one of the basic tastes. But how convincing is the experimental evidence?
Is it really time to declare fat the sixth taste?