A study found that semaglutide, a compound widely used to treat obesity and diabetes, improved the physical, metabolic, and cognitive functions of aged mice and even extended their lifespan. Semaglutide is the main ingredient in the obesity drug Wegovy and the diabetes drug Ozempic.
Researchers at the University of California administered semaglutide or saline to 20-month-old female mice and published the findings on health status and lifespan on the 3rd in the journal Nature.
Semaglutide is a drug that mimics the action of glucagon-like peptide-1 (GLP-1), a hormone secreted in the gut. After meals, GLP-1 signals satiety to the brain to reduce appetite, and when blood sugar rises, it helps insulin secretion. Semaglutide stimulates the GLP-1 receptor on which this hormone acts to regulate food intake and blood glucose.
Recently, studies have suggested that GLP-1 drugs may go beyond weight loss to lower the risks of cardiovascular, kidney, and liver diseases and potentially affect neurodegenerative disorders. However, it remains unclear whether these effects are merely secondary to weight loss or the result of GLP-1 signaling itself acting directly on multiple organs.
The researchers examined what actual effects semaglutide has on the health and lifespan of mice. In the experiment, the median lifespan of mice given continuous semaglutide was 834 days, 92 days, or about 12%, longer than the control group's 742 days. Median lifespan refers to the lifespan at the point when half of the subjects have died and half remain alive.
Not only lifespan but also activity and cognitive function improved. Mice administered semaglutide for three months moved more actively and explored their surroundings in a new environment. Spatial memory and blood glucose regulation also improved.
In the semaglutide group, multiple aging markers—including chronic inflammation, cellular senescence, mitochondrial dysfunction, and stem cell decline—also improved. In particular, in muscle, activity of genes related to mitochondria, the cell's energy producers, and energy production increased, suggesting a possible partial recovery of age-related declines in muscle function. In the brain, in the dentate gyrus of the hippocampus, which is important for memory and learning, markers related to neural stem cell activity and the generation of new neurons increased.
The team also checked whether these changes were simply due to eating less. Mice given semaglutide reduced their food intake by about 24%, and the researchers compared some health and aging markers with mice whose calorie intake was restricted to a similar level. While some similar changes appeared in both groups, the semaglutide group showed better results than the calorie-restricted group in measures such as exploratory behavior, spatial memory, and blood glucose regulation.
The researchers said, "Some of semaglutide's effects are related to reduced calorie intake, but that alone is not enough to explain all the changes," adding, "It is possible that stimulating the GLP-1 receptor itself affects physiological functions related to aging."
Professor Lee Sang-yeol of Kyunghee University School of Medicine said of the study, "Semaglutide showed the potential to slow aging by influencing how the body takes in and regulates nutrients and energy, beyond its effect on reducing weight."
Still, it is premature to take these results to mean semaglutide slows human aging or extends lifespan. The researchers noted, "To confirm whether GLP-1 drugs actually affect human aging and lifespan, long-term clinical trials are necessary," and added, "It also needs to be verified separately whether there is benefit for older adults without obesity or aging-related diseases."
Lee also added, "Based on these results alone, semaglutide should not be used to slow aging in thin older adults with low muscle mass," and said, "We need to confirm through clinical trials and real-world clinical data what effects and side effects appear when the drug is administered to older adults over a long period."
References
Nature (2026), DOI: https://doi.org/10.1038/s41586-026-10940-7