Diabetes medication may alter how the brain responds to food RESEARCH
A study presented at the American Diabetes Association's 75th Scientific Sessions shows that gut hormone-based medications used to treat diabetes, such as GLP-1 receptor agonists, may alter the brain's response to food, possibly reducing cravings and increasing satisfaction while eating.
Previous studies have shown that the brains of obese people have a greater response to pictures of food than those of lean people, and a reduced reward response during the consumption of food, which may lead to overeating.
Researchers in Amsterdam tested the hypothesis that the GLP-1 receptor agonist exenatide—a medication which mimics the effects of natural GLP-1 by binding to the GLP-1 receptor—was helping patients with type 2 diabetes lose weight by altering the brain's response to food consumption and decreasing appetite.
"When you eat, there are several hormones released. GLP-1 is one of them," said Liselotte van Bloemendaal, a PhD student at the Diabetes Center, VU University Medical Center in Amsterdam. These hormones relay information to the central nervous system about nutritional status to regulate appetite. Using functional MRIs, which measure brain activity by detecting changes in blood flow, the researchers looked at the reward centers in the brains of obese individuals with and without type 2 diabetes and measured the response to the anticipation of and drinking of chocolate milk while being given GLP-1 receptor agonist intravenously versus placebo. They found that GLP-1 receptor activation decreased anticipatory food reward, which may reduce cravings, and increased the feeling of food reward during consumption, which may reduce overeating.
According to Bloemendaal, further investigation is needed to study whether adding a second hormone—such as glucagon—to GLP-1 receptor agonist treatment could further increase weight loss. The U.S. Food and Drug Administration recently approved the first GLP-1 agonist for the treatment of obesity in the United States.
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