The newest experimental weight-loss drugs, such as retatrutide, do not stop at the celebrated GLP-1 and GIP pathways: they also activate receptors for glucagon, a hormone that textbooks associate chiefly with raising blood sugar. Jonathan Campbell, associate professor of medicine at Duke University School of Medicine, argues that this third ingredient may be central to why the drugs perform so strikingly well in trials.
Campbell, who studies metabolism and diabetes, presented the thinking at the American Diabetes Association's Scientific Sessions in June 2026. Emerging evidence suggests that activating glucagon receptors increases the energy the body uses, and that the hormone helps the body process nutrients, burn fat and respond to insulin after meals: a far richer physiological role than its classical reputation as a simple counterweight to insulin would allow.
The implications matter for an obesity field moving at remarkable speed. If glucagon's contribution can be understood and tuned, drug developers could design agents that pair appetite suppression with genuinely increased energy expenditure, rather than relying on reduced food intake alone. Duke's metabolism researchers are now working to pin down precisely how the hormone reshapes the body's handling of fuel after a meal.