Enzyme inhibitor aids muscle repair in semaglutide-treated mice
In obese male mice, adding an enzyme inhibitor during five weeks of semaglutide treatment improved recovery after muscle injury without compromising weight loss.
Our read
Interventions- Studied:
- Experiments in young adult obese male mice, 2 wk postinjury, against mice receiving semaglutide alone
- What changed:
- Adding PGDHi increased muscle strength after injury in semaglutide-treated obese mice compared with semaglutide alone
- The catch:
- Muscle recovery was assessed only 2 wk after injury, leaving longer-term recovery unmeasured
- Stake:
- An author founded Merrifield Therapeutics and holds shares in it. Authors hold patents with Epirium Bio.
- In the record:
- One of 1,741 papers on semaglutide on record: 694 with results in people, 92 in animals. Its result on muscle mass agrees with all 4 other findings on record.
Editor of record: Boris Djordjevic · AgingResearch.News
Male C57BL/6J mice made obese by 12 weeks on a high-fat diet received semaglutide, an enzyme inhibitor, both drugs or control injections in a randomized animal experiment. Daily injections delivered semaglutide at 120 micrograms per kilogram and the inhibitor, SW033291, at 5 milligrams per kilogram for five weeks. The inhibitor targeted 15-PGDH, an enzyme that increases with injury and aging.
After three weeks, researchers injured calf muscles and assessed recovery two weeks later. Semaglutide alone reduced muscle mass without reducing strength, but regenerating muscle fibers were smaller. Adding the inhibitor improved fiber growth and strength recovery compared with semaglutide alone, without compromising weight loss. In muscles examined five days after injury, the combination also increased the number of dividing muscle stem cells, which help repair muscle.
Why it matters
Muscle supports mobility and metabolic health. The work points to an enzyme that increases with aging as a potential target for supporting muscle recovery during weight loss.
Caveats
The experiment tested recovery from toxin-induced muscle injury in young adult male mice with diet-induced obesity, not age-related muscle decline in older animals or people.
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