Don't Like Broccoli? A Receptor Gene's Variation Suggests An Evolutionary Excuse

Main Category: Nutrition / Diet
Also Included In: Biology / Biochemistry
Article Date: 21 Sep 2006 - 4:00 PDT

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By testing the bitterness perceived by individuals possessing different versions of the same taste receptor, researchers have obtained new evidence supporting the idea that evolution of the receptor gene has shaped avoidance of certain vegetables that can inhibit thyroid function. The findings are reported by Mari Hakala and Paul Breslin of Monell Chemical Sciences Center in Philadelphia, Pennsylvania and appear in the September 19th issue of Current Biology, published by Cell Press.

Compounds known as glucosinolates are present in a variety of vegetables included in the human diet (especially Cruciferous vegetables), but these compounds can block the formation of organic iodine and the transport of iodine into the thyroid. Iodine is necessary for proper thyroid function, and in geographic regions where inorganic iodine levels are low, endemic goiter (enlarged thyroid) can arise in response to the need to maintain levels of thyroid hormone. In such circumstances, thyroid toxins such as glucosinolates can exacerbate problems with thyroid function. Deficiencies in thyroid function can result in retarded sexual maturation and mental retardation in low-iodine regions (typically, remote areas far from the sea).

Past work has suggested that evolution of the TAS2R family of bitter taste receptors has been shaped by the potential advantage of avoiding certain toxic compounds in plants, but the evidence thus far has been based on findings that used synthetic bitter compounds. For example, past work showed that people possessing genetically different versions of a particular TAS2R receptor exhibit correspondingly different sensitivities to the bitter compounds phenylthiocarbamide (PTC) and propylthiouracil (PROP), which resemble glucosinolates.

In the new work, researchers were able to show that different genetic versions of this same receptor, known as hTAS2R38, specifically determine people's perception of plants that synthesize glucosinolates. In their experiments, the researchers divided a test array of vegetables into those that contain glucosinolates, such as broccoli and turnips, and those that do not contain known glucosinolates. The researchers found that individuals possessing two copies of a "sensitive" version of the hTAS2R38 gene rated the glucosinolate-containing vegetables as 60% more bitter than did subjects possessing two copies of an "insensitive" version of the receptor gene. In comparison, individuals possessing one copy of each version of the gene rated the bitterness of glucosinolate-containing vegetables at an intermediate level.

The researchers found that the differences in bitterness perception by the "sensitive" and "insensitive" hTAS2R38 groups reached statistical significance for six vegetables: watercress, mustard greens, turnip, broccoli, rutabaga, and horseradish.

Though iodine supplementation aids significantly in ameliorating thyroid problems in low-iodine areas, the researchers note that over 1 billion people worldwide are at risk, in principle, for thyroid insufficiency--this reflects the likelihood that strong selective pressures in the past have shaped our ability to detect anti-thyroid compounds and avoid them, especially in low-iodine regions. The new findings illustrate the importance of individual taste receptor genes in shaping our perception of foods and, the researchers point out, show that variation in even a single gene can impact how people perceive an entire family of vegetables.

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The researchers include Mari A. Sandell and Paul A.S. Breslin of Monell Chemical Senses Center in Philadelphia, Pennsylvania. This work was supported by grants from NIH DC02995 and P50 DC06760 to P.A.S.B.

Sandell et al.: "Variability in a taste-receptor gene determines whether we taste toxins in food." Publishing in Current Biology Vol 16 No 18, R792-4. DOI 10.1016/j.cub.2006.08.049. www.http://www.current-biology.com/

Contact: Heidi Hardman
Cell Press

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