Don't care for broccoli? A receptor gene's variation suggests an evolutionary excuse

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

Contact: Heidi Hardman
Cell Press

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