Photo used for illustrative purposes.
Eating biscuits, cakes, burgers and sausage rolls makes us fat by delaying digestion, according to new research.
Junk food rewires the brain by reducing our ability to regulate appetite, scientists have said.
The discovery could open the door to an anti-obesity pill that targets neurons.
Experiments in rats found the cells called astrocytes control a chemical pathway to the gut. But the study suggests that continuously gorging on fatty and sugary products disrupts it.
Lead author Dr Kirsteen Browning, of Penn State University in the US, said: “Calorie intake seems to be regulated in the short-term by astrocytes.
“We found a brief exposure of high fat/calorie diet has the greatest effect on astrocytes - triggering the normal signalling pathway to control the stomach.
“Over time astrocytes seem to desensitise to the high fat food.
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“After around 10-14 days of eating high fat/calorie diet, astrocytes seem to fail to react and the brain’s ability to regulate calorie intake seems to be lost.
“This disrupts the signalling to the stomach and delays how it empties.”
Understanding the brain’s role and the complex mechanisms that lead to gluttony may lead to therapies to treat weight gain.
Almost two in three adults in the UK and a third of children are overweight or obese - raising their risk of cardiovascular disease and type 2 diabetes.
Astrocytes initially react when junk food is ingested - releasing chemicals called gliotransmitters.
They stimulate neurons that ensure the stomach contracts correctly to fill and empty in response to food passing through the digestive system.
When astrocytes are inhibited, the cascade is disrupted. The decrease in signalling chemicals leads to a delay in digestion because the stomach doesn’t fill and empty appropriately.
The vigorous investigation used behavioural observation to monitor food intake in more than 200 lab rodents fed either a normal or high fat diet for one, three, five or 14 days.
This was combined with pharmacological and specialist genetic techniquwa to target distinct neural circuits.
It enabled the US team to specifically inhibit astrocytes in a particular region of the brainstem - the posterior part that connects to the spinal cord.
They assessed how individual neurons behaved when the rats were awake.
If the same mechanism occurs in humans the mechanism could be safely targeted providing other neural pathways are not affected.
Dr Browning said: “We have yet to find out whether the loss of astrocyte activity and the signalling mechanism is the cause of overeating or that it occurs in response to the overeating.
“We are eager to find out whether it is possible to reactivate the brain’s apparent lost ability to regulate calorie intake. If this is the case, it could lead to interventions to help restore calorie regulation in humans.”
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