A new animal study indicates that food calories, not just sweetness, can trigger a positive response in the brain - a breakthrough that could have implications for anti-obesity strategies and the food industry.
Scientists have long known that there is a link between sweet taste and production of dopamine, a neurotransmitter that provokes feelings of pleasure. Dopamine is produce in two areas of the brain - the nucleus accumbens (NAcc) of the ventral striatum, and the orbitofrontal cortex (OFC).
However the researchers from Duke University Medical Center in Durham, North Carolina, wanted to find out if the brain dopamine reward system is sensitive to the metabolic value of nutrients, even when the taste receptor activation is absent.
From their animal study they found that calorific content of a food substance triggered dopamine response in the NAcc area even in mice that were modified to have no capacity for taste.
This result, if it also holds true for humans, could have significant impact for the strategies to combat the global obesity epidemic - and particularly the food industry's efforts to help address the problem.
To date, reformulation of food products along healthier lines has revolved around making products that have less sugar, fat or salt, but as far as possible the same taste as the original product.
This is because consumers are unlikely to buy a product again if they do not like the taste. This is particularly important when it comes to sweet foods, as the consumer does not want to feel they are losing out on a treat.
However the new study suggests that simply replicating the taste might not be enough to satisfy cravings for the high calorie snacks we are used to. In the long run this could have an effect on people's ability to stick with a diet or healthier eating approach.
First author Ivan de Araujo and his team carried out behavioural, neurochemical and electrophysiological experiments on taste-blind mice - that is, mice that had been bred to have no capacity for taste - and compared the findings with normal mice.
In the first part of the study the team provided the mice with two feeding bottles, one containing water and the other containing sucrose (sugar) solution.
Initially the taste blind mice showed no preference, but after a time they showed a preference for licking the sweet solution.
The researchers then repeated the experiment, this time using water in one bottle and a solution of the sweetener sucralose, which has the same sweetness as sugar but without the calories.
In this case the taste-blind mice showed no preference for the sucralose solution over the water. The indication is that, in the first instance, it was the calories that attracted the mice to the sugar.
In both experiments normal mice preferred the sweet solutions over the water, as would be expected.
The researchers then turned their attention to what is actually happening at a neural level. They implanted the mice with microdyalysis probes, so they could see whether the behaviour they had observed was related to dopamine secretion levels.
They found that in the taste-blind mice, the NAcc area responded to only after they had licked the sugar solution, not the sucralose solution. In addition, there was no activity ion the OFC region after either solution was consumed.
In the normal mice, on the other hand, both the NAcc and the OFC released dopamine after intake of sugar and sucralose.
The indication here is that the NAcc responds to sweet taste and calorific content, whereas the OFC responds only to sweet taste.
"Our results demonstrate that even in the absence of taste transduction or palatability, caloric intake produces measurable tonic increases in NAcc dopamine," wrote de Araujo and his colleagues.
"Thus, both palatability and postingestive factors can independently increase dopamine levels in brain reward circuits."
Neuron DOI: 10.1016/j.neuron.2008.01.032
"Food Reward in the absence of taste receptor signalling"
Authors: Ivan Araujo, Albino Oliviera-Maia, Tatyana Sotnikova, Raul Gainetdinov, Marc Caron, Miguel Nicolelis, Sidney Simon.