If you were asked to distinguish between cheese and chocolate, I doubt there would be much difficulty—if someone replaced your Hershey’s square on a s’more with a slice of Gouda, you would notice right away.
While the distinction between sweet and savory may seem quite obvious, the science is surprisingly similar—and yet complicated. Right now, researchers see the divide between these tastes as thinly balanced between two amino acids in particular: glutamate and aspartate. This post is the first of a three-part series, I which I explore the history and science of these two seemingly “opposite” taste experiences—savory (umami) and sweet—and their relationship to the two amino acids listed above. I’m curious about what the history of two common food additives, monosodium glutamate (MSG) and aspartame, can teach us about how small variations between structure can affect the taste perception of sweet and savory.
Before I get to the subtle (yet important) differences between sweet and savory tastes, let’s establish how our bodies are currently understood to taste at all. Let’s consider this scenario: you’re smelling your grandma’s freshly baked chocolate cookies. “Taste” proper does not actually begin with mastication (chewing), but rather in the combination of the olfactory and gustatory cortexes. In everyday English, that means what you smell now can affect what you taste later. That sweet, homey aroma flooding your nose and making you drool is part of the complex chemosensory relationship between taste and smell (see Taste perception, associated hormonal modulation, and nutrient intake). Olfactory nerves, stimulated by this sugary bouquet, flood your brain with “signals” that in turn relay information to the gustatory (taste) cortex. So before you even begin indulging grandma’s secret recipe, your body is already preparing for what’s to come based on smell alone (See Food-Related Odors Activate Dopaminergic Brain Areas). When you finally satisfy your cravings, gustatory cells clustered on your taste buds send information to your brain once again (See Taste perception, associated hormonal modulation, and nutrient intake) and you perceive sweetness.
It is here on the taste buds where “flavor” begins. Umami and sweetness are perceived by Type II G-proteins coupled cells in the gustatory complex of the mouth. On these cells, families of taste receptors (TAS1Rs) perceive different sensations. There are three types of these heterodimer TAS1Rs: TAS1R1, TAS1R2, and TAS1R3. Savory (umami) tastes are sensed by both TAS1R1 and TAS1R3, while sweetness is perceived by TAS1R2 and TAS1R3. In a study dealing with mice that lack TAS1R3 (the taste receptor for both umami and sweetness), signs of perception for both umami and sweetness existed, hinting that the separate taste receptors (TAS1R2 and TAS1R1) were specific for umami and sweetness (See The endocrinology of taste receptors). A recent study on rats without the required transient taste receptors and calcium modulators for sweetness and umami also revealed the importance of ATP in both umami and sweetness perception. Type II cells communicate taste to the gustatory cortex via ATP release, which helps increase enteroendocrine (in this case that means taste receptors inside the gut) hormone release that can cause changes in appetite and satiety. What is interesting to note here is that the perception of and response to sweet and savory tastes are almost identical.
So why are umami and sweetness so different? What is it about the glutamate in MSG and the aspartic acid in aspartame make them taste so different? The beginning of this answer is found in the TAS1R1 and TAS1R2 receptors. If we examine the structure of aspartate (a component of aspartame) and glutamate (a component of MSG), we would find the difference between these two acidic compounds is as small as an extra methylene on glutamate. No big deal, right? In fact, in the molecular world, a carbon and two hydrogen can greatly affect orientational binding in corresponding receptors—a small difference in structure makes a big difference in how a molecule affects the body. As found in the study above, TAS1R1 is responsible for the umami taste. The TAS1R1 and TAS1R3 receptors in a heterodimeric formation (this means these two receptors combine and work together in a one collective unit) can bind specifically to L-glutamine, which is the foundational amino acid in MSG and umami-tasting foods (See Glutamine Triggers and Potentiates Glucagon-Like Peptide-1 Secretion by Raising Cytosolic Ca2+ and cAMP).
In a recent study on Old World Monkey, researchers demonstrated that TAS1R2 coupled with TAS1R3 was the heterodimer required to perceive sweetness in both natural and artificial sweeteners. The same study demonstrated that aspartame specifically interacted with the “Venus Flytrap Module” (insert plain English translation) of TAS1R2 receptors. This complex binding is still being researched, yet it appears to act in the same way as a fly landing on a Venus Flytrap. Aspartate can interact with TAS1R2, which then binds and “closes,” sending “sweetness” signals to the brain. Both TAS1R1 and TAS1R2, however, remain a puzzle to researchers.
So I’m not the only one with questions left about savoriness, sweetness, and taste perception in general. How exactly taste receptors coordinate to the brain continues to be researched. Yet what has been found is that small differences in molecular structure have a big impact on taste. Glutamate and aspartate are practically the same amino acid, but each one relays a different taste perception to the brain. For now, it is clear that in food there is much more that meets the eye (and the tongue for that matter!).
References to check out!
Calvo, S. S. C., & Egan, J. M. (2015). The endocrinology of taste receptors. Nature Reviews Endocrinology, 11(4), 213.
Loper, H. B., La Sala, M., Dotson, C., & Steinle, N. (2015). Taste perception, associated hormonal modulation, and nutrient intake. Nutrition reviews, 73(2), 83-91.
Sorokowska, A., Schoen, K., Hummel, C., Han, P., Warr, J., & Hummel, T. (2017). Food-related odors activate dopaminergic brain areas. Frontiers in human neuroscience, 11, 625.
Tolhurst, G., Zheng, Y., Parker, H. E., Habib, A. M., Reimann, F., & Gribble, F. M. (2011). Glutamine triggers and potentiates glucagon-like peptide-1 secretion by raising cytosolic Ca2+ and cAMP. Endocrinology, 152(2), 405-413.