Researchers discovered that metformin, a medication commonly used to treat diabetes, might help reduce airway inflammation in people who have both asthma and obesity. Using mice with obesity-related asthma, scientists found that metformin reduced swelling and irritation in the airways by activating a protective protein in the body and turning off inflammatory signals. This finding is exciting because current asthma treatments don’t work as well for overweight people, and metformin is already a safe, affordable medication that millions of people take. If these results hold true in humans, it could offer a new treatment option for the millions of people struggling with both conditions.

The Quick Take

  • What they studied: Whether metformin, a common diabetes medicine, could reduce airway swelling and inflammation in mice that had both obesity and asthma
  • Who participated: Laboratory mice were divided into groups: some with normal weight and asthma, some with obesity and asthma, and some treated with metformin. The exact number of mice wasn’t specified in the abstract
  • Key finding: Metformin significantly reduced airway inflammation markers and swelling in obese asthmatic mice. The drug activated a protective protein called AMPK and shut down inflammatory pathways, reducing harmful inflammatory chemicals by more than 50% (P < 0.05)
  • What it means for you: This suggests metformin might become a helpful additional treatment for people with both obesity and asthma, but human studies are needed first. Don’t start taking metformin for asthma without talking to your doctor—this is early-stage research

The Research Details

Scientists created mice with obesity-related asthma by feeding them a high-fat diet and exposing them to a protein that triggers asthma symptoms. They then treated some mice with metformin and compared the results across different groups. Researchers measured inflammation in the lungs using multiple methods: they looked at lung tissue under a microscope, measured inflammatory chemicals in the blood, and analyzed how genes were being expressed using molecular techniques. This multi-method approach helped them understand both what was happening in the lungs and the biological mechanisms behind it.

This research approach is important because it doesn’t just show that metformin helps—it reveals how it works. By studying the specific proteins and chemical signals involved, scientists can better understand whether this effect would likely happen in humans and whether metformin could be safely combined with existing asthma treatments. The combination of looking at physical changes in lung tissue plus measuring molecular changes provides strong evidence for the mechanism

This is laboratory research in mice, which is an important first step but not the same as human studies. The findings are statistically significant (P < 0.05 means there’s less than a 5% chance the results happened by accident), and the study used multiple measurement methods to confirm results. However, mice don’t always respond the same way humans do, so human clinical trials would be needed before this could become a treatment recommendation

What the Results Show

Mice with obesity and asthma showed much worse airway inflammation than mice with normal weight and asthma. When these obese asthmatic mice were treated with metformin, their airway inflammation improved significantly. The drug worked by activating a protein called AMPK, which acts like a cellular ‘master switch’ that reduces inflammation. At the same time, metformin shut down a harmful inflammatory pathway called NLRP3, which normally triggers the release of inflammatory chemicals. The levels of three key inflammatory chemicals—IL-1β, IL-18, and leptin—all decreased substantially after metformin treatment. These improvements were consistent across multiple measurements, suggesting the effect was real and reproducible.

The study found that obesity made asthma worse by increasing the number of immune cells called eosinophils in the airways. Metformin reduced these elevated immune cell counts. The drug also reduced leptin, a hormone produced by fat cells that contributes to inflammation. This suggests metformin may work partly by reducing the inflammatory signals that come from excess body fat itself, not just by treating the asthma directly

Previous research has shown that obesity worsens asthma and makes standard treatments less effective. This study builds on that knowledge by identifying a specific mechanism and a potential solution. Metformin has been studied for other inflammatory conditions, but this appears to be focused research on its specific effects on obesity-related asthma. The AMPK/NLRP3 pathway has been implicated in other inflammatory diseases, so this finding fits with existing scientific understanding

This research was conducted only in mice, not humans, so results may not translate directly. The study doesn’t specify exactly how many mice were used, making it harder to assess statistical power. The research doesn’t compare metformin to other potential treatments or to standard asthma medications. Long-term effects weren’t studied—we only know what happened during the treatment period. Additionally, mice with experimentally-induced obesity and asthma may not perfectly mirror the human condition, which develops over years with multiple contributing factors

The Bottom Line

This research suggests metformin may help reduce asthma symptoms in people with obesity, but it’s too early to recommend it as a treatment. Current confidence level: Low to Moderate (this is animal research only). If you have both obesity and asthma, continue taking your prescribed asthma medications and talk to your doctor about weight management strategies. Do not start metformin for asthma without medical supervision—it requires a prescription and monitoring

People with both obesity and asthma who find their current treatments aren’t working well should be aware of this research and discuss it with their doctor. Researchers studying asthma and obesity should follow up with human clinical trials. People taking metformin for diabetes should not assume it’s treating their asthma. People with asthma alone or normal weight should not expect the same benefits

In this mouse study, improvements appeared relatively quickly after metformin treatment began. However, in humans, benefits would likely take weeks to months to become noticeable. Any human trials would need to run for several months to properly assess effectiveness and safety

Want to Apply This Research?

  • If prescribed metformin by your doctor, track daily asthma symptoms using a simple 1-10 scale (1=no symptoms, 10=severe), along with rescue inhaler use frequency and peak flow measurements if you have a meter. Record weekly weight and note any changes in shortness of breath during normal activities
  • Work with your healthcare provider to implement a structured program combining metformin (if prescribed), weight management through diet and exercise, and consistent asthma medication use. Use the app to log meals, exercise minutes, and asthma control to identify patterns between weight changes and symptom improvement
  • Establish a baseline of current asthma control before any changes. Track symptoms weekly for at least 8-12 weeks to see if metformin (if prescribed) helps. Monitor weight monthly rather than daily to see long-term trends. Share this data with your doctor at regular appointments to assess whether the treatment is working and adjust as needed

This research was conducted in laboratory mice and has not been tested in humans. Metformin is a prescription medication that requires medical supervision and is not approved for asthma treatment. Do not start, stop, or change any asthma or diabetes medications without consulting your healthcare provider. If you have both asthma and obesity, work with your doctor to develop a comprehensive treatment plan. This summary is for educational purposes only and should not be considered medical advice. Always consult with qualified healthcare professionals before making any changes to your treatment regimen.