Sweetness

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Sweet foods, such as this strawberry shortcake, are often eaten for dessert.

Sweetness is a basic taste most commonly perceived when eating foods rich in sugars. Sweet tastes are generally regarded as pleasurable. In addition to sugars like sucrose, many other chemical compounds are sweet, including aldehydes, ketones, and sugar alcohols. Some are sweet at very low concentrations, allowing their use as non-caloric sugar substitutes. Such non-sugar sweeteners include saccharin, aspartame, and sucralose. Other compounds, such as miraculin, may alter perception of sweetness itself.

The perceived intensity of sugars and high-potency sweeteners, such as aspartame and neohesperidin dihydrochalcone, are heritable, with gene effect accounting for approximately 30% of the variation.[1]

The chemosensory basis for detecting sweetness, which varies between both individuals and species, has only begun to be understood since the late 20th century. One theoretical model of sweetness is the multipoint attachment theory, which involves multiple binding sites between a sweetness receptor and a sweet substance.

Studies indicate that responsiveness to sugars and sweetness has very ancient evolutionary beginnings, being manifest as

taste recognition threshold, being detectable at around 1 part in 200 of sucrose in solution. By comparison, bitterness appears to have the lowest detection threshold, at about 1 part in 2 million for quinine in solution.[5] In the natural settings that human primate ancestors evolved in, sweetness intensity should indicate energy density, while bitterness tends to indicate toxicity.[6][7][8] The high sweetness detection threshold and low bitterness detection threshold would have predisposed our primate ancestors to seek out sweet-tasting (and energy-dense) foods and avoid bitter-tasting foods. Even amongst leaf-eating primates, there is a tendency to prefer immature leaves, which tend to be higher in protein and lower in fibre and poisons than mature leaves.[9] The "sweet tooth" thus has an ancient heritage, and while food processing has changed consumption patterns,[10][11] human physiology remains largely unchanged.[12]

Examples of sweet substances

A great diversity of chemical compounds, such as aldehydes and ketones, are sweet. Among common biological substances, all of the simple carbohydrates are sweet to at least some degree. Sucrose (table sugar) is the prototypical example of a sweet substance. Sucrose in solution has a sweetness perception rating of 1, and other substances are rated relative to this.[13] For example, another sugar, fructose, is somewhat sweeter, being rated at 1.7 times the sweetness of sucrose.[13] Some of the amino acids are mildly sweet: alanine, glycine, and serine are the sweetest. Some other amino acids are perceived as both sweet and bitter.

The sweetness of 5% solution of glycine in water compares to a solution of 5.6% glucose or 2.6% fructose.[14]

A number of plant species produce

chicken eggs
, is also sweet.

Sweetness of various compounds[14][15][16][17][18][19][20]
Name Type of compound Sweetness
Lactose Disaccharide 0.16
Maltose Disaccharide 0.33 – 0.45
Trehalose (α,α-trehalose) Disaccharide max. 0,45[21]
Isomaltulose Disaccharide 40 - 50[22]
Sorbitol
Polyalcohol
0.6
Galactose Monosaccharide 0.65
Glucose Monosaccharide 0.74 – 0.8
Glycine Amino acid 0.6 – 0.86
Sucrose Disaccharide 1.00 (reference)
Xylitol sugar alcohol 1,02[23]
Fructose Monosaccharide 1.17 – 1.75
Sodium cyclamate Sulfonate 26
Steviol glycoside Glycoside 40 – 300
Aspartame
methyl ester
180 – 250
Acesulfame potassium Oxathiazinone dioxide 200
Sodium saccharin
Sulfonyl
300 – 675
Sucralose Modified disaccharide 600
Thaumatin Protein 2000
Neotame Aspartame analog 8000
Sucrooctate Guanidine 162,000 (estimated)
Bernardame Guanidine 188,000 (estimated)
Sucrononic acid Guanidine 200,000 (estimated)
Carrelame Guanidine 200,000 (estimated)
Lugduname Guanidine 230,000 (estimated)

Some variation in values is not uncommon between various studies. Such variations may arise from a range of methodological variables, from sampling to analysis and interpretation. Indeed, the taste index of 1, assigned to reference substances such as sucrose (for sweetness), hydrochloric acid (for sourness), quinine (for bitterness), and sodium chloride (for saltiness), is itself arbitrary for practical purposes.[18] Some values, such as those for maltose and glucose, vary little. Others, such as aspartame and sodium saccharin, have much larger variation.

Even some inorganic compounds are sweet, including beryllium chloride and lead(II) acetate. The latter may have contributed to lead poisoning among the ancient Roman aristocracy: the Roman delicacy sapa was prepared by boiling soured wine (containing acetic acid) in lead pots.[24]

Hundreds of synthetic organic compounds are known to be sweet, but only a few of these are legally permitted[where?] as food additives. For example, chloroform, nitrobenzene, and ethylene glycol are sweet, but also toxic. Saccharin, cyclamate, aspartame, acesulfame potassium, sucralose, alitame, and neotame are commonly used.[citation needed]

Sweetness modifiers

Boys Pilfering Molasses – On The Quays, New Orleans, 1853 painting by George Henry Hall

A few substances alter the way sweet taste is perceived. One class of these inhibits the perception of sweet tastes, whether from sugars or from highly potent sweeteners. Commercially, the most important of these is

jellies
and other fruit preserves to bring out their fruit flavors by suppressing their otherwise strong sweetness.

Two natural products have been documented to have similar sweetness-inhibiting properties:

diabetes mellitus
.

On the other hand, two plant proteins,

sour
foods to taste sweet. Once the tongue has been exposed to either of these proteins, sourness is perceived as sweetness for up to an hour afterwards. While curculin has some innate sweet taste of its own, miraculin is by itself quite tasteless.

The sweetness receptor

Sweetness is perceived by the taste buds.

Despite the wide variety of chemical substances known to be sweet, and knowledge that the ability to perceive sweet taste must reside in taste buds on the tongue, the biomolecular mechanism of sweet taste was sufficiently elusive that as recently as the 1990s, there was some doubt whether any single "sweetness receptor" actually exists.

The breakthrough for the present understanding of sweetness occurred in 2001, when experiments with

G-protein coupled receptor that is the sweetness receptor in mammals.[29]

Human studies have shown that sweet taste receptors are not only found in the tongue, but also in the lining of the gastrointestinal tract as well as the nasal epithelium, pancreatic islet cells, sperm and testes.[30] It is proposed that the presence of sweet taste receptors in the GI tract controls the feeling of hunger and satiety.

Another research has shown that the threshold of sweet taste perception is in direct correlation with the time of day. This is believed to be the consequence of oscillating leptin levels in blood that may impact the overall sweetness of food. Scientists hypothesize that this is an evolutionary relict of diurnal animals like humans.[31]

Sweetness perception may differ between species significantly. For example, even amongst the primates sweetness is quite variable. New World monkeys do not find aspartame sweet, while Old World monkeys and apes (including most humans) all do.[32] Felids like domestic cats cannot perceive sweetness at all.[33] The ability to taste sweetness often atrophies genetically in species of carnivores who do not eat sweet foods like fruits, including bottlenose dolphins, sea lions, spotted hyenas and fossas.

Sweet receptor pathway

To depolarize the cell, and ultimately generate a response, the body uses different cells in the taste bud that each express a receptor for the perception of sweet, sour, salty, bitter or umami. Downstream of the taste receptor, the taste cells for sweet, bitter and umami share the same intracellular signalling pathway.[34] Incoming sweet molecules bind to their receptors, which causes a conformational change in the molecule. This change activates the G-protein, gustducin, which in turn activates phospholipase C to generate inositol trisphosphate (IP3), this subsequently opens the IP3-receptor and induces calcium release from the endoplasmic reticulum. This increase in intracellular calcium activates the TRPM5 channel and induces cellular depolarization.[35][36] The ATP release channel CALHM1 gets activated by the depolarization and releases ATP neurotransmitter which activates the afferent neurons innervating the taste bud.[37][38]

Cognition

The color of food can affect sweetness perception. Adding more red color to a drink increases its perceived sweetness. In a study darker colored solutions were rated 2–10% higher than lighter ones despite having 1% less sucrose concentration.[39] The effect of color is believed to be due to cognitive expectations.[40] Some odors smell sweet and memory confuses whether sweetness was tasted or smelled.[41]

Historical theories

Lugduname is the sweetest chemical known.

The development of

molecular weights
were often sweeter than the larger compounds.

In 1919, Oertly and Myers proposed a more elaborate theory based on a then-current theory of color in synthetic dyes. They hypothesized that to be sweet, a compound must contain one each of two classes of structural motif, a glucophore and an auxogluc. Based on those compounds known to be sweet at the time, they proposed a list of six candidate glucophores and nine auxoglucs.

From these beginnings in the early 20th century, the theory of sweetness enjoyed little further academic attention until 1963, when

Lewis base (B) separated by about 0.3 nanometres
. According to this theory, the AH-B unit of a sweetener binds with a corresponding AH-B unit on the biological sweetness receptor to produce the sensation of sweetness.

B-X theory was proposed by

hydrophobicity and sweetness. This theory formalized these observations by proposing that to be sweet, a compound must have a third binding site (labeled X) that could interact with a hydrophobic site on the sweetness receptor via London dispersion forces
. Later researchers have statistically analyzed the distances between the presumed AH, B, and X sites in several families of sweet substances to estimate the distances between these interaction sites on the sweetness receptor.

MPA theory

The most elaborate theory of sweetness to date is the multipoint attachment theory (MPA) proposed by Jean-Marie Tinti and Claude Nofre in 1991. This theory involves a total of eight interaction sites between a sweetener and the sweetness receptor, although not all sweeteners interact with all eight sites.[42] This model has successfully directed efforts aimed at finding highly potent sweeteners, including the most potent family of sweeteners known to date, the guanidine sweeteners. The most potent of these, lugduname, is about 225,000 times sweeter than sucrose.

References

Cited

  1. PMID 26181574
    .
  2. ^ Blass, E.M. Opioids, sweets and a mechanism for positive affect: Broad motivational implications. (Dobbing 1987, pp. 115–124)
  3. PMID 4745817
    .
  4. .
  5. ^ McAleer, N. (1985). The Body Almanac: Mind-boggling facts about today's human body and high-tech medicine. New York: Doubleday.
  6. ^ Altman, S. (1989). "The monkey and the fig: A Socratic dialogue on evolutionary themes". American Scientist. 77: 256–263.
  7. ^ Johns, T. (1990). With Bitter Herbs They Shall Eat It: Chemical ecology and the origins of human diet and medicine. Tucson: University of Arizona Press.
  8. ^ Logue, A.W. (1986). The Psychology of Eating and Drinking. New York: W.H. Freeman.
  9. ^ Jones, S.; Martin, R.; Pilbeam, D. (1994). The Cambridge Encyclopedia of Human Evolution. Cambridge: Cambridge University Press.
  10. S2CID 143766021
    .
  11. ^ Fischler, C. Attitudes towards sugar and sweetness in historical and social perspective. (Dobbing 1987, pp. 83–98)
  12. PMID 8351513
    .
  13. ^ a b Guyton, Arthur C. (1991). Textbook of Medical Physiology (8th ed.). Philadelphia: W.B. Saunders.
  14. ^
  15. .
  16. .
  17. . Retrieved 14 September 2010.
  18. ^ .
  19. ^ Dermer, OC (1947). "The Science of Taste". Proceedings of the Oklahoma Academy of Science. 27: 15–18.
  20. .
  21. ^ O'Brien-Nabors, Lyn, ed. (2012). Alternative sweeteners (4th ed.). Boca Raton: CRC Press. ISBN 978-1-4398-4614-8. Retrieved 25 June 2014.
  22. ^ "Herstellung fermentierter Getränke unter Verwendung von Isomaltulose". d-nb.info. 2011-04-13. p. 16. Retrieved 2023-12-10.
  23. .
  24. .
  25. .
  26. .
  27. .
  28. .
  29. .
  30. .
  31. .
  32. ^ Biello, David (August 16, 2007). "Strange but True: Cats Cannot Taste Sweets". Scientific American. Archived from the original on March 19, 2011. Retrieved July 28, 2009.
  33. PMID 20696704
    .
  34. .
  35. .
  36. .
  37. .
  38. .
  39. .
  40. .
  41. .

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