Late-Life Semaglutide Extended Lifespan in Female Mice, Study Finds
A Nature study found that semaglutide improved muscle, cognition and several aging-related measures in older female mice, while treatment continued until death was associated with a median lifespan nearly 100 days longer than in untreated animals. The findings are preclinical and do not establish a longevity benefit for humans.

Semaglutide extended the lifespan of older female mice and improved several measures of physical and cognitive function in a study published in Nature. The researchers compared the GLP-1 drug with calorie restriction to examine whether its effects were explained primarily by reduced food intake.
Led by Danica Chen of the University of California, Berkeley, the study treated 20-month-old female mice with semaglutide for three months. Compared with untreated controls, the animals showed better muscle and cognitive function. Gene-expression analysis also indicated reductions in several features associated with natural aging, including increased inflammation and diminished regenerative capacity.
In a separate group that received semaglutide until the end of life, the treated mice had a median lifespan nearly 100 days longer than untreated animals. The source report describes these results as evidence that the drug may affect physiological aging in healthy older mice, rather than only delaying individual age-related diseases.
The researchers then tested how semaglutide compared with a restricted diet. For five months, one group of 20-month-old female mice received semaglutide, while another was placed on a diet providing 24% fewer calories and matched the treated animals’ feeding pattern. Many physiological measurements were similar between the groups.
Some differences emerged. Mice receiving semaglutide exceeded baseline levels in exploratory behavior, spatial memory and blood-sugar maintenance. Their metabolic rate also remained largely unchanged, whereas it fell in the calorie-restricted animals. The findings led the researchers to propose that GLP-1 drugs could influence a biological pathway that is not identical to calorie restriction, although that possibility remains a direction for future research rather than an established mechanism.
Rafael de Cabo of the National Institute on Aging, who authored a commentary on the study, said that if GLP-1 agonists slow the aging process, their broad effects on chronic disease would be consistent with that possibility. The study’s authors likewise said the results could inform future investigations into longevity-related interventions.
The work was conducted in healthy older female mice, however, and does not show that semaglutide extends human lifespan. The source report notes that additional clinical studies will be needed to assess whether GLP-1 drugs have longevity effects in people, including healthy older adults. A post-hoc analysis of the SLIM LIVER trial was cited as part of the emerging human evidence, but the animal findings themselves do not establish clinical efficacy for longevity.
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