Scientists may have found a mechanism that controls our sense of satiety

Scientists may have found a mechanism that controls our sense of satiety

Swedish researchers may have found an unknown mechanism that controls our sense of satiety. It gives hope for future remedies for obesity and diabetes.

Healthy people who say they experience satisfaction and saturation after a meal have high levels of Ghrelin before a meal, and very low after a meal. Obese people, on the other hand, have medium levels both before and after meals.

Researchers at the University of Gothenburg may have found a mechanism that suppresses saturation signals from the small intestine. This may explain both saturation disorders in obesity and diabetes, and in part, the rapid health effects of gastric bypass obesity surgery.

The enzyme that triggers the formation of ketone bodies

The study is performed on gastric bypass-operated patients, as well as on mice and cell cultures. What the researchers found is a mechanism in the small intestine that can explain how saturation signalling is inhibited, and the culprit is an enzyme that triggers the formation of ketone bodies in the intestinal mucosa, which in turn places the hormone-producing cells in order.

The hormone GLP-1, which is typically released from the gastrointestinal mucosa when eating, is inhibited by diabetes and obesity, which is considered to be an essential causative mechanism behind the diseases.

Several modern anti-diabetic and overweight medications are copies of GLP-1 in which attempts have been made to mimic regular release through injections.

A new type of drug

Instead of injecting copies of GLP-1, a preparation that blocks the enzyme in the gut could be added, thereby removing the saturation hormone brake.

“Such a drug could mimic the effect of a gastric bypass operation,” says Ville Wallenius, associate professor and chief physician of gastro-surgery, and the lead author of the study.

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