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After short periods of feeding a diet high in fat and calories, the brain adapts to react to what is eaten and reduces the amount of food eaten to balance calorie intake.
This was determined by a new investigation in rats published in The Journal of Physiology by professionals from the Penn State College of Medicine in the United States.
The researchers suggest that the calorie intake is regulated in the short term by cells called astrocytes (large star-shaped cells in the brain that regulate many different functions of neurons in the brain) that control the signaling pathway between the brain and the gut.
In fact, continually eating a diet high in fat and calories appears to disrupt this signaling pathway.
Obesity starts in the brain
According to studies, understanding the role of the brain and the complex mechanisms that lead to overeating, a behavior that can lead to weight gain and obesity, could help develop therapies to treat it.
Obesity is currently a global public health problem. This pathology is associated with increased risk of cardiovascular disease and type 2 diabetes.
63% of adults consider themselves to be over a healthy weight and around half of them live with obesity in England. While one in three children who finish elementary school is overweight or obese, according to Neuroscience News.
“Calorie intake seems to be regulated in the short term by astrocytes. We discovered that brief exposure (3 to 5 days) to a high-fat, high-calorie diet has the greatest effect on astrocytes, which activates the normal signaling pathway to control the stomach,” said Dr. Kirsteen Browning, of the Penn State College of Medicine.
In addition, he explained that over time, astrocytes seem to lose sensitivity to high-fat foods, since after about 10 to 14 days of eating a diet high in fat and calories, they seem to not react.
They determined that the brain’s ability to regulate calorie intake appears to be lost and therefore signaling to the stomach is disrupted and delays the way it empties.
Human studies need to be done to confirm if it occurs in the same way, and if so, further testing will be required to assess whether the mechanism could be safely targeted without disrupting other neural pathways.
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