The sweet taste of lemon

August 16th, 2022

Written by: Omer Zeliger

There’s nothing more satisfying than a perfect cold lemonade on a hot summer day; not too sweet and not too sour. Our ability to taste lets us enjoy delicious food and drink, but taste isn’t just for fun – it gives our body valuable information about what we’re eating. When we drink that lemonade, our sour taste cells tell us about the lemon’s acidity1, and our sweet taste cells tell us that we’re eating something sugary and energy-rich2.

This sense isn’t perfect; just like optical illusions trick our eyes into seeing things that aren’t there, “taste illusions” can confuse our tongues into thinking we’re eating something we’re not. Any time we use artificial sweeteners, we trick our tongues into thinking we’re eating more sugar than we actually are. Another example is the miracle berry, also known as Synsepalum dulcificum. For around an hour after eating this berry, anything that would normally taste sour tastes sweet instead3. How does the miracle berry transform taste and trick our tongue? The answer comes from how our taste buds detect chemicals in the environment and transform that information into nervous activity.

Hundreds of taste buds cover the tongue, each of which holds dozens of taste cells4. Each taste cell responds to only one specific type of taste. For example, bitter cells will respond to bitter-tasting food but not to sour food. When a cell detects its preferred taste on the tongue, it fires an electric signal to tell the nervous system what it found. Finally, the brain detects which taste cells have fired and turns that into the experience of taste.

Of the five commonly accepted taste cell types (sweet, salty, sour, bitter, and umami, though others have been theorized), sweet is one of the better-understood cell types. Sweet cells have receptors on their surface that are able to bind to and detect sugars in the environment5. When enough of these receptors are bound, the cell is activated – and then, when the sugar has washed away, the receptors unbind and the cell stops its activity. See figure 1 for the full process of how sweet signals reach the brain.

Figure 1. The pathway from sugar to sweet taste. When we eat something containing sugar, the sugar molecules enter our taste buds and activate sweet receptors on our sweet taste cells (1). These cells send electrical impulses through the nervous system to the brain (2), which interprets the electrical activity as a sweet taste (3). Created with BioRender.com.

Miracle berries trick sweet cell receptors into thinking that they detect sugar with the help of a deceptive chemical called miraculin. To understand how miraculin causes such an effect, scientists exposed cells that have the sweet receptor to miraculin and measured their electrical activity under several conditions3. When scientists gave the cells only miraculin they found low activity, which would mean that miraculin doesn’t activate sweet cells on its own. However, when the scientists added a weak acid to the mixture, mimicking what happens when you eat sour food, the sweet cells greatly increased their electrical activity – the more acidic it was, the more active they were. In the body, this “sweet” activity would travel to the brain and tell it that you were eating something sweet, even though the activity was triggered sour food and there was no sugar present.

Another interesting finding of the study was that miraculin blocks the cells from responding to real sugar. The scientists discovered this by comparing the cells’ activity when they got just sugar to when they got a combination of sugar and miraculin. In non-acidic environments (where miraculin can’t activate sweet cells) the cells that got the miraculin/sugar combo were less active than those that got just sugar, indicating that the miraculin stopped the sweet receptors from reacting to sugar.

We still don’t know exactly how miraculin causes this fake sweet activity, but the prevailing theory (illustrated in figure 2) is that miraculin binds to sweet receptors and latches on to them, staying on your tongue for up to an hour after eating a berry3. Even though it binds to the receptor, miraculin still can’t activate the sweet receptors under normal conditions, making the miraculin on the tongue tasteless and undetectable. However, when you eat sour food and make your mouth slightly more acidic, the miraculin changes its shape to activate the sweet receptors, creating the illusion that sour food tastes sweet. The theory is bolstered by miraculin’s ability to prevent sugar from binding to the receptors, suggesting that miraculin being already bound may block the receptor from binding to sugar as well.

Figure 2. The sweet receptor will normally bind sugar (left). By binding to the sweet receptor without activating it (middle left), miraculin can change its shape to activate the receptor (middle right) and block sugar from binding to the receptor (right). Created with BioRender.com.

With miraculin’s natural sweetening properties, could it be used as an alternative sweetener similar to Splenda or Sweet’N Low? It’s possible, but there needs to be more research. We don’t know if miraculin is any better than other sweeteners at copying the taste of real sugar or if it avoids any of the health risks of other sweeteners (though one group of scientists have found that miracle fruit may have anti-diabetic properties6). For now, the FDA has banned miraculin as a food additive in the United States, though it is still legal to sell miracle berries or to grow them yourself7. Regardless, miracle berries are an interesting phenomenon that make us question why we taste the way we do.

References

  1. Teng, B., Wilson, C. E., Tu, Y. H., Joshi, N. R., Kinnamon, S. C., & Liman, E. R. (2019). Cellular and Neural Responses to Sour Stimuli Require the Proton Channel Otop1. Current biology : CB, 29(21), 3647–3656.e5.
  2. Nelson, G., Hoon, M. A., Chandrashekar, J., Zhang, Y., Ryba, N. J., & Zuker, C. S. (2001). Mammalian sweet taste receptors. Cell, 106(3), 381–390.
  3. Misaka T. (2013). Molecular mechanisms of the action of miraculin, a taste-modifying protein. Seminars in cell & developmental biology, 24(3), 222–225.
  4. Roper, S. D., & Chaudhari, N. (2017). Taste buds: cells, signals and synapses. Nature reviews. Neuroscience, 18(8), 485–497.
  5. Zhao, G. Q., Zhang, Y., Hoon, M. A., Chandrashekar, J., Erlenbach, I., Ryba, N. J., & Zuker, C. S. (2003). The receptors for mammalian sweet and umami taste. Cell, 115(3), 255–266.
  6. Han, Y. C., Wu, J. Y., & Wang, C. K. (2019). Modulatory effects of miracle fruit ethanolic extracts on glucose uptake through the insulin signaling pathway in C2C12 mouse myotubes cells. Food science & nutrition, 7(3), 1035–1042.
  7. Izawa, K., Amino, Y., Kohmura, M., Ueda, Y., & Kuroda, M. (2010). 4.16 – Human–Environment Interactions – Taste. In L. Mander & H.-W. Liu (Eds.), Comprehensive natural products II: Chemistry and biology (Vol. 4, pp. 631–671). essay, Elsevier.

Cover image by RitaE via Pixabay.

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