Junk food’s evil ways: High-fat diet hijacks the brain’s ability to regulate appetite
HERSHEY, Pa. — Eating fatty foods like burgers and fried chicken can obviously lead to obesity, but not in the way you may think. Researchers say a high-fat diet and junk food rewires the brain, reduces our ability to regulate appetite and regulate calorie consumption.
The discovery could open the door to an anti-obesity pill that targets neurons in the brain. Experiments in rats show that cells called astrocytes control a chemical pathway to the gut. However, the study suggests that continuously gorging on fatty and sugary products disrupts that link.
“Calorie intake seems to be regulated in the short-term by astrocytes. We found that a brief exposure (three to five days) of high fat/calorie diet has the greatest effect on astrocytes, triggering the normal signaling pathway to control the stomach. Over time, astrocytes seem to desensitize to the high fat food. 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 signaling to the stomach and delays how it empties,” says lead author Dr. Kirsteen Browning from Penn State College of Medicine, in a media release.
Understanding the brain’s role and the complex mechanisms that lead to gluttony may lead to therapies to treat weight gain. The CDC estimates that over 40 percent of U.S. adults are obese, raising their risk of cardiovascular disease and Type 2 diabetes.
What happens in the brain after consuming a high-fat diet?
Astrocytes initially react when someone consumes junk food, 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 something inhibits astrocytes, it disrupts the cascade. The decrease in signaling chemicals leads to a delay in digestion because the stomach doesn’t fill and empty appropriately. The vigorous investigation used behavioral 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.
Study authors combined this with pharmacological and specialist genetic techniques to target distinct neural circuits. This enabled the team to specifically inhibit astrocytes in a particular region of the brainstem, the posterior part that connects to the spinal cord.
Researchers then assessed how individual neurons behaved when the rats were awake. If the same mechanism occurs in humans, drugs could safely target the mechanism, providing the treatment doesn’t affect other neural pathways.
“We have yet to find out whether the loss of astrocyte activity and the signaling 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,” Dr. Browning concludes.
The findings appear in The Journal of Physiology.
South West News Service writer Mark Waghorn contributed to this report.