By Kyj Mandzy, Bellarmine University
Everyone likes sweets, but it is truly staggering to see to what extent they enjoy them. The average person in an industrialized country consumes 33.1kg of sugar a year. This accounts for a daily intake of 260 calories from sugar alone every single day, roughly one-eighth of the energy the average individual needs for a day. Neuroimaging of the brain reveals that sugar consumption results in a dopamine release in the nucleus accumbens (an area associated with motivation, novelty, and reward). Similar responses are elicited from the consumption of cocaine and heroin. The desire for sweetness itself is primal. Studies indicate that the responsiveness to sugars and sweetness has very ancient evolutionary beginnings, being manifest as chemotaxis even in motile bacteria such as E. coli.
The taste map of the tongue showing different parts of the tongue as responsible for each basic taste is a common misconception. Receptors for each of the basic tastes are actually found in each taste bud. Sweetness is detected by a variety of G protein coupled receptors coupled to the G protein gustducin found on the taste buds. Incoming sweet molecules bind to their receptors, which causes a conformational change in the molecule. The change activates the gustducin, which in turn activates adenylate cyclase catalyzing the conversion of ATP to cAMP. The cAMP molecule then ultimately closes a potassium ion channel. The excess potassium ions increase and depolarize the cell which causes a neurotransmitter release, which is then received by a primary afferent neuron. The individual then perceives a sweet taste.
Measurement of perceived sweetness is based on sucrose, with all sweeteners rated relative to sucrose. Most chemical sweeteners such as stevia or aspartame have sweetness indexes in the low two hundreds while sucrose has a sweetness index of 1. Instead of adding gratuitous amounts of sugar, manufactures are able to add a small amount of much more potent sweetener to achieve the same effect. Interestingly, there is a substance with an estimated sweetness index of 300,000, Lugduname, a guanadine compound synthesized in Lyons University. There are also compounds which can alter a person’s perception of how sweet a substance is. I can readily attest to their prowess. After taking Miraculin, (a protein found in berries that can alter taste perception) I tasted food completely differently. I was eating lemons much like someone would eat an apple.
There are two taste-modifying protiens, Curculin and Miraculin, which change the percieved sweetness of foods. Curculin is isolated from the fruit of Curculigo latifolia (Weevil-Wort), a plant from Malaysia. It also acts as sweetener by itself. Ingestion of Curculin results in a perception of food being sweetened with a 12% sucrose solution. The effects of taking Curculin last roughly 5 minutes. Miraculin is extracted from the fruit of Synsepalum dulcificum (Miracle fruit) a berry from West Africa. It is the more known taste-modifying protein and is readily available for purchase online. Ingestion of Miraculin results in a perception of food being sweetened with a 17% sucrose solution. The effects of taking Miraculin last roughly 20 minutes. Their mechanisms are not fully understood but possible models have been presented.
The current model of Curculin is based on its two active sites working in tandem. It is believed that one active site of Curculin strongly binds to the taste receptor membranes; the second active site then fits into the sweet receptor site. The fitting in the sweet receptor site allows for an easier induction of sweetness. Miraculin is thought to have a more invasive mechanism changing the structure of taste receptors on the cells of the tongue. As a result, the sweet receptors are activated by acids turning lemons sweet. The two histidine residues (29 and 59) appear to be mainly responsible for the taste-modifying behavior. Similar to Curculin, one site maintains the attachment of the protein to the membranes while the other activates the sweet receptor itself. Further research on Miraculin is being conducted at the University of Tokyo.
Depending on the results of future studies, Curculin and Miraculin may provide new alternatives to sweeteners found in sodas and junk food. The possibility of diet aids is also present with the two proteins helping consumers overcome their sweet tooth. With growing concern over diets and negative eating habits in this country, healthier alternatives are increasingly significant.
Blass, E.M. Opioids, sweets and a mechanism for positive affect: Broad motivational implications. (Dobbing 1987, pp. 115–124)
Chen, J.; Pattarawarapan, M.; Zhang, A. J.; Burgess, K. (2000). “Solution- and Solid-Phase Syntheses of Substituted Guanidinocarboxylic Acids”. Journal of Combinatorial Chemistry 2 (3): 276–281. doi:10.1021/cc990084b.
Ito K, Asakura T, Morita Y, Nakajima K, Koizumi A, Shimizu-Ibuka A, Masuda K, Ishiguro M, Terada T, Maruyama J, Kitamoto K, Misaka T, Abe K (August 2007). “Microbial production of sensory-active miraculin”. Biochem. Biophys. Res. Commun. 360 (2): 407–11. doi:10.1016/j.bbrc.2007.06.064. PMID 17592723.
Joesten, Melvin D; Hogg, John L; Castellion, Mary E (2007). “Sweeteness Relative to Sucrose (table)”. The World of Chemistry: Essentials (4th ed.). Belmont, California: Thomson Brooks/Cole. p. 359. ISBN 0-495-01213-0.
Kurihara, Y. 1992. Characteristics of antisweet substances, sweet proteins, and sweetness-inducing proteins. Crit. Rev. Food Sci. Nutr. 32:231-252
Yamashita H, Akabane T, Kurihara Y (April 1995). “Activity and stability of a new sweet protein with taste-modifying action, curculin”. Chem. Senses 20 (2): 239–43. doi:10.1093/chemse/20.2.239. PMID 7583017.