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How Sensitive to Sweet Are You?

New Taste Study Says Your Ability to Decipher ‘Sweet’ Relies Heavily on Two Letters in Your Genetic Code
July 17, 2009

If you’re someone who likes to load up on sugar during your mid-morning coffee, 3:00 p.m. work break, and late-night snack, your genes might be trying to tell you something. You may be less sensitive to the taste of sweet than other people.

New research published in the June 25 online issue of Current Biology has found that our ability to detect sweetness not only depends on the taste receptors occupying our taste buds, but it also has a lot to do with two small bits of DNA hiding in our genetic code that regulate sweet taste receptor levels. The research is funded by the National Institute on Deafness and Other Communication Disorders (NIDCD), one of the National Institutes of Health.

Researchers Dennis Drayna, Ph.D., chief of the Section on Systems Biology of Communication Disorders in NIDCD’s Laboratory of Molecular Genetics, and research fellow Alexey Fushan, Ph.D., along with researchers from Givaudan Flavors Corporation, Cincinnati, and University of Virginia, Charlottesville, have found that two very small variations in a person’s DNA—called single nucleotide polymorphisms, or SNPs—upstream of the sweet taste receptor subunit gene TAS1R3 play a big role in determining whether or not a person is sensitive to the taste of sugar. What’s more, they found that the frequency of the two possible variants in these SNPs differs by population, such that people of European ancestry are more likely to be more sensitive to the taste of sweet while people of African ancestry are more likely to have a reduced sensitivity.

SNPs occur normally in our DNA and they are the most common type of genetic variation among people. Each SNP represents a difference in a single DNA building block, called a nucleotide. There are four possible nucleotides, which are customarily abbreviated as the first letter in their name: adenine (A), thymine (T), guanine (G), and cytosine (C).

For the study, the researchers measured the sensitivity to sweet taste in 144 volunteers. Ninety-two were of European ancestry, 37 were of Asian ancestry, and 15 were of African ancestry. For each volunteer, they provided nine samples of sugar solution in varying concentrations, and asked them to arrange the samples from low to high concentration. Not only were the scientists interested in the lowest concentration for which a person could taste sweet (their threshold), but they also wanted to know how well they could decipher the changes between concentrations. The volunteers were then assigned a score based on how well they did.

Next, for each volunteer, the researchers sequenced the nucleotides of the two genes on chromosome 1 that encode the sweet receptor subunits TAS1R2 and TAS1R3, plus small sections of DNA upstream and downstream. Although they found no correlation between any individual genetic variant in TAS1R2 and taste sensitivity, they found 2 SNPs upstream of TAS1R3, at positions -1266 and -1572, that strongly correlated with their scores. In both SNPs, volunteers who possessed a C were generally more sensitive to sweet taste, while volunteers who possessed a T in those locations were generally less sensitive to sweet. Because a DNA molecule contains two copies of each gene, a person who is homozygous C/C would be more sensitive to sweet than a person who is heterozygous C/T, who, in turn, would be more sensitive than a person who is homozygous T/T. Likewise, two C’s at both positions would make a person more sensitive to the taste of sweet in comparison to two C’s at one position and a C and a T at the second position. Overall, they found that volunteers who were heterozygous C/T exhibited a 25 percent decrease in sugar sensitivity whereas volunteers who were homozygous T/T experienced a 50 percent decrease.

The researchers then wanted to learn more about the effect that the two SNPs were having on TAS1R3. They created variants of the upstream region of the TAS1R3 gene—where the gene’s controls are housed—and attached them to a small ring of DNA, or plasmid, containing luciferase. Luciferase is an enzyme that gives fireflies their glow, and scientists can use it as a way to tell if a gene is expressed, or made into a protein. They introduced the luciferase plasmid into two cell lines that are known to express the TAS1R3 gene, in this case, human intestinal cancer cells. (Interestingly, the same receptors that taste sweet on our tongue also recognize sugars in our intestines.) If the controls are switched on at full tilt, the luciferase will make lots of proteins, which will light up strongly, telling us that the gene is fully expressed. If the controls are working at lower capacity, then fewer proteins will yield a dimmer light, telling us that the gene’s expression is reduced. As suspected, they found that the presence of a T in one or both of the SNPs resulted in reduced gene expression.

Our genes account for roughly half of what we experience when we taste sweet; the rest may be attributed to aging, hormones, our diet, and other factors. The researchers suggest that, of the 50 percent that is genetic, the two SNPs account for roughly 16 percent of the variability within the population.

In addition, the researchers report that there is a distinctive gradient of the two nucleotides across Eurasia, with Europeans having the lowest frequencies of the T nucleotide, Asians having medium frequencies, and sub-Saharan African populations having the largest frequencies. They hypothesize that the reason for the difference may be that people in northern climates had less access to carbohydrate-rich vegetation, and, for this reason, they may have developed a higher sensitivity to sugar at low concentrations.


Last Updated Date: 
July 17, 2009