The hundreds of receptors that give us our sense of smell have been found to have important roles in other parts of the body, and the prospect of targeting them with drugs is growing.
The main constraint on Hatt’s exploration of olfactory receptors around the body has been the fact that many of them are orphan receptors — there are no known molecules that activate them. Because identifying activating chemical messengers is intensive work, without guaranteed success, his laboratory has favoured studying receptors with known activators — leaving hundreds of extra-nasal receptors uncharacterized.
Consequently, many researchers in the field want to change the terminology used to describe these receptors. ‘Extra-nasal’ represents one straightforward and descriptive solution, and is what Hanns Hatt, a physiologist at Ruhr University of Bochum in Germany, has chosen to use in his most recent papers. Di Pizio has proposed the term ‘ecnomotopic’, from Greek words meaning ‘out of the usual place’.
Four years later, Pluznick and her colleagues showed that one olfactory receptor called Olfr78, found in certain mouse kidney cells, was activated by short-chain fatty acids such as acetate and propionate. They then demonstrated that SCFA stimulation mediated the release of the hormone renin, which leads to vasoconstriction.
The olfactory biologist he contacted was sceptical, Ley says. But seeing that around 100 of the more than 400 known human olfactory receptors can be expressed by macrophages, Ley began to investigate. Knowing that a ligand for the receptor must be present in the serum they used to grow the liver cells, Wang and his team soon found the culprit: asprosin, a peptide hormone that had been discovered in 2016.
Resolving this biological question will take many years of dedicated evolutionary research. But the peptide discoveries might have more practical implications in the short term for those seeking to develop therapies aimed at olfactory receptors.
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