Swedish scientists have identified specific neurons in the brain which may drive over-eating behaviour.
The researchers at Stockholm’s Karolinska Institutet investigated the neural activity underlying the consumption of fatty and sugary foods and activity levels – and examined the effect of a specific cluster of neurons in the brain’s emotional centre, the amygdala, on energy consumption and energy expenditure.
In their study, published in Nature Neuroscience, they tested this by turning these brain cells ‘on’ and ‘off’ in genetically engineered mice – and discovered that a group of neurons in the amygdala (a part of the brain involved in experiencing emotions and decision-making) may also trigger hedonic eating.
The researchers conducted several experiments on mice to observe their neuronal behaviour: first they observed neural activity in response to eating regular chow or a high-fat diet (HFD) after food restriction; after an HFD, but not chow, they noted higher activity levels among certain neurons in a part of the amygdala known as the interstitial nucleus of the posterior limb of the anterior commissure (IPAC).
The findings indicated certain neurons of the IPAC ‘may be activated following consumption of palatable food, and not necessarily an energy deficit’. Further tests demonstrated these IPAC neurons could also be activated in the presence of fatty and sugary food and smells in the absence of hunger.
Researchers then experimented to see whether activating these neurons would lead to over-feeding, and found ‘switching’ the neurons ‘on’ increased sated mice’s intake of all foods and liquids; however the effect was larger for coconut and olive oil-flavoured HFDs and white chocolate, than for chow and dark chocolate, while switching the neurons ‘off’ then resulted in reduced feeding.
Finally, the researchers tested whether inhibition of the neurons in the IPAC could prevent obesity, by inhibiting IPAC activity in some mice and not others, and then feeding them an obesity-inducing diet over several weeks.
After 6 weeks eating in a ‘diet-inducing obesity’, control mice became obese, whereas other mice remained lean; and those with inhibited IPAC activity had a higher lipid oxidation rate (the speed at which fat is burned), higher energy expenditure and engaged in more exercise. IPAC-inhibited mice also had lower blood sugar levels than controls.
The researchers concluded inactivation of specific neurons in the IPAC protects against obesity and related health conditions by promoting metabolic changes that benefit energy expenditure.
Study co-author Professor Alessandro Furlan told medicalnewstoday.com: ‘The identification of the neuronal substrates mediating over-eating could provide new molecular targets for devising new anti-obesity treatments.’
