Chowing down on the likes of burgers, sausage rolls and sweet treats makes us pile on the podge by delaying digestion, new research has revealed.
Scientists stateside at the Penn State University found that junk food rewires the brain, in-turn reducing our ability to regulate appetite.
They also added that bombshell breakthrough could open the door to an anti-obesity pill, which works by targeting neurons.
Hull Live reports that 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, 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.
"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 research team's 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 techniques 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 added: "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."
The study was published in The Journal of Physiology.
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