Obesity Conference-NFOD 2026

Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted by intestinal L-cells in response to nutrient intake and plays a central role in the regulation of glucose homeostasis and energy balance. In obesity, dysregulation of appetite control, impaired satiety signaling, and altered gut–brain communication contribute to excessive energy intake and weight gain. GLP-1 acts as a key metabolic regulator by enhancing glucose-dependent insulin secretion, suppressing glucagon release, delaying gastric emptying, and promoting satiety through both peripheral and central mechanisms.

In the context of obesity, GLP-1 has gained significant clinical relevance due to its ability to modulate appetite and food intake via the gut–brain axis. It communicates with the central nervous system through vagal afferent pathways and direct action on hypothalamic nuclei, particularly those involved in hunger and satiety regulation. This results in reduced appetite, decreased caloric consumption, and improved energy homeostasis. Additionally, GLP-1 influences reward-related eating behavior by modulating dopaminergic signaling pathways, further contributing to reduced hedonic feeding.

Pharmacological GLP-1 receptor agonists, such as semaglutide and liraglutide, have demonstrated substantial efficacy in obesity management, producing significant and sustained weight reduction along with improvements in cardiometabolic risk factors. More recently, dual and multi-agonist therapies targeting GLP-1 in combination with other metabolic pathways have further expanded therapeutic potential. Overall, GLP-1 represents a pivotal advancement in obesity treatment by addressing both metabolic dysfunction and central appetite regulation, making it a cornerstone of modern