Long-term exposure to unpalatable flavours can increase the later acceptance of foods containing such ingredients by modifiying neurones that are involved in taste perception, according to new research carried out in fruit flies.
The study, published in Nature Neuroscience, uncovers how the taste preferences of fruit flies are modified by experience – something that the researchers behind the study suggest is among the most widely observed, but poorly understood modifiable behavioural phenomena.
Led by Professor Craig Montell from the University of California at Santa Barbara, the team note that the ability to shift taste preferences is essential for survival, because animals from insects to humans have to respond to a changing food environment.
Indeed, the US-based researchers noted that alterations in taste are well known in humans, as people from the Far East have different taste preferences than people from the West – while individuals who move from one culture to another typically learn to accept the local foods, some of which were originally aversive.
Now, using the fruit fly, Drosophila melanogaster, as an animal model, the team aimed to unravel the mechanisms behind how animals modify their taste preferences in this way.
“We show that dietary exposure to an unappealing but safe additive, camphor, caused the fruit fly Drosophila melanogaster to decrease camphor rejection,” explained the researchers.
The fruit flies' reduced distaste for camphor occurred through a mechanism that involves the degradation of the TRPL protein by an enzyme called E3 ubiquitin ligase, or Ube3a, which targets specific protein substrates for degradation.
Following the decline in TRPL, there was also a decrease in synaptic connections, but that was not sufficient to cause the taste adaptation., said the authors.
"We don't know what's activating the Ube3a, but it's tantalizing to speculate that it is calcium regulated," Montell added. "We think it's a combination of the decline in TRPL levels and the decrease in synaptic connections that together cause the change in behaviour.”
"We not only found that ubiquination is important and leads to degradation, but we also discovered that mutations in Ube3a prevent this taste plasticity," he continued. "This is because in the absence of Ube3a, TRPL is not ubiquinated so it is not degraded. This underscores that it's the decline in the TRPL levels that underlie this mechanism."
An interesting phenomenon was the reversibility of the process of accepting camphor as a food additive, the team added – noting a decline in TRPL levels and synaptic connections that accompany the flies' increased acceptance of camphor reverse after returning the flies long-term to a camphor-free diet.
For humans this might translate to mean that repeated exposure to disliked food over a period of weeks or months may result in the eventual acceptance of that food.
These findings not only show the molecular and cellular pathway that controls how diet changes taste proclivity in an animal, but also suggest a general neural mechanism underlying food experience-induced changes in taste preferences in other animals, including mammals.
"Our work raises the possibility that reversible changes in taste receptor cells, as a result of long-term exposure to a specific diet, could contribute to a similar type of phenomenon in humans," concluded Montell.
"If we come to understand this really well, someday it could be harnessed by the food industry."