Within this repository of bitter taste information, notable ligands such as PTC (phenylthiocarbamide) and PROP ( 6-n-propylthiouracil) have been extensively studied and are widely recognized.
The range of ligands recognized by the T2R38 receptor adds to our understanding of the complex molecular interactions involved in the perception of bitter taste.
Bitter taste receptors that are expressed in extra-oral tissues fill a variety of functional physiological roles.
[10] TAS2R38 is expressed in many tissues, such as human sinonasal epithelial cells, airway smooth muscle, monocytes, macrophages, heart, arteries, thyroid, skin, etc.
Several studies have suggested, however, that the AVI polymorphism may code for an entirely new receptor which processes a different and as-yet undiscovered bitter compound.
[16] For an evolutionary perspective, the reference sequences for gorillas and chimps have the PAV haplotype, while mouse and rat have PAI.
[16] The perceived bitterness of cruciferous vegetables, such as broccoli, results from glucosinolates and their hydrolysis products, particularly isothiocyanates and other sulfur-containing compounds.
[18] Preliminary research indicates that genetic inheritance through the gene TAS2R38 may be responsible in part for bitter taste perception in broccoli.
The genetic variation is involved with consumption of fruits, sweets and fat, it was shown in a research that non-tasters had higher intake of these food products that might lead to obesity.
Other ligands that activate T2R38 are N-Acyl homoserine lactones (AHLs) are a class of signaling molecules involved in bacterial quorum sensing.
[23] Notably, a correlation has been observed between medically refractory chronic rhinosinusitis (CRS) and nonprotective genetic variants of the TAS2R38 gene.
Certain polymorphisms associated with TAS2R38 have been linked to decreased incidence of allergies, asthma, nasal polyposis, aspirin sensitivity, and diabetes among CRS patients, although statistical significance has not yet been established.