Antibiotics are powerful tools against bacterial infections, but their effectiveness is declining as antibiotic-resistant bacteria continue to emerge. A new study from the UNC School of Medicine reveals that people with diabetes are particularly vulnerable to developing antibiotic-resistant strains of Staphylococcus aureus—a leading cause of drug-resistant infections and deaths. Their findings, published in Science Advances, highlight how diabetes accelerates bacterial resistance and suggest strategies for combatting it.
Diabetes impairs blood sugar regulation, often leading to excess glucose in the bloodstream. This high-sugar environment creates ideal conditions for Staph bacteria to thrive and multiply rapidly. At the same time, diabetes weakens the immune system, reducing the body’s ability to control infection.
As bacterial populations grow, random mutations occur. Some mutations grant resistance to antibiotics, and in people with diabetes, these resistant strains quickly dominate due to the abundance of glucose and the lack of immune defences. Staphylococcus aureus is uniquely suited to take advantage of this diabetic environment. Once a resistant mutation appears, it rapidly takes over the entire infection.
Study researchers used a diabetic mouse model infected with S. aureus. The researchers divided mice into two groups: one received a compound to induce diabetes, while the other remained non-diabetic. Both groups were then infected with S. aureus and treated with rifampicin, an antibiotic known for its high resistance rates.
The results were alarming. In non-diabetic mice, rifampicin effectively eliminated the infection. In diabetic mice, rifampicin had little effect, and within just four days, the infection was dominated by highly resistant Staph strains—over 100 million rifampicin-resistant bacteria. When resistant bacteria were introduced deliberately, they quickly overran the infection in diabetic mice but remained a minority in non-diabetic models.
These findings indicate that diabetes not only increases susceptibility to infection but also accelerates the development of antibiotic resistance, posing a serious public health concern.
If diabetes drives antibiotic resistance, could controlling blood sugar help prevent it? The researchers tested this hypothesis by administering insulin to diabetic mice. Remarkably, insulin treatment normalised blood sugar levels, slowed bacterial growth and significantly reduced the emergence of resistant strains. This suggests that resistance and its spread are not only linked to drug prescription but also to the health status of those taking antibiotics. By controlling blood glucose, the rapid proliferation of resistant bacteria was prevented.
Recognising the broader implications of their findings, study authors are now expanding their research to other vulnerable populations, including chemotherapy patients and transplant recipients, to determine if they also experience accelerated antibiotic resistance. They are also investigating other antibiotic-resistant bacteria, such as Enterococcus faecalis, Pseudomonas aeruginosa, and Streptococcus pyogenes.
With antibiotic resistance on the rise, understanding how underlying health conditions contribute to the problem is critical. This research underscores the importance of managing chronic diseases like diabetes—not only for individual health but also as a strategy to combat the growing threat of antibiotic resistance.
Source: UNC School of Medicine
Image Credit: National Institute of Allergy and Infectious Diseases
References:
Shook JC et al. (2025) Diabetes potentiates the emergence and expansion of antibiotic resistance. Science Advances. 11(7).
