Researchers have determined the glucagon-like peptide 1, or GLP-1, appetite-suppressing hormone systems found in the gut and brain act independently of each other to control eating, according to a news release from the University of Florida.
Additionally, stimulating both systems together further reduces food consumption. The findings could have far-reaching implications for developing new medicines designed to treat obesity.
Food calories trigger the release of GLP-1 in both the gut and brain. It’s been inaccurately assumed that gut GLP-1 prompts communication between the gut and brain GLP-1 to control how much to eat. However, in a recent study published in Nature Metabolism, a team of researchers from the UF College of Pharmacy, Florida State University and University College in London found the gut and brain GLP-1 systems do not interact. Rather, they suppress eating via independent circuits.
The finding comes at a time when the prevalence of obesity is increasing and GLP-1 has taken on new importance. Interventions such as bariatric surgery have been shown to increase GLP-1 levels in obese patients after a meal. Meanwhile, new medications aimed at increasing GLP-1 levels are being developed to promote weight loss and improve other obesity-related health risks.
UF researchers also tested whether GLP-1 cells in the brain are activated by the GLP-1-based, anti-obesity medications liraglutide and semaglutide. They found both medications suppress eating but do not activate brain GLP-1 cells. This comes on the heels of a recent study published in the New England Journal of Medicine that found the diabetes medication semaglutide resulted in significant weight loss in obesity patients.
