Your browser is no longer supported

For the best possible experience using our website we recommend you upgrade to a newer version or another browser.

Your browser appears to have cookies disabled. For the best experience of this website, please enable cookies in your browser

We'll assume we have your consent to use cookies, for example so you won't need to log in each time you visit our site.
Learn more

Immune system link to type-2 diabetes

  • 1 Comment

A type of immune system cell plays a key role in the development of type-2 diabetes, research suggests.

Neutrophils, which normally attack bacteria and other foreign invaders, also secrete a protein that promotes insulin resistance, scientists found.

The condition, which occurs when the body stops responding to the blood sugar-regulating hormone insulin, is one of the main features of type-2 diabetes.

Neutrophils appear to promote chronic low-grade inflammation, increasing the chances of insulin resistance.

“These results are largely unexpected,” said US researcher Dr Da Young Oh, of the University of California at San Diego, US.

“Although several immune cells have been established in the aetiology (origin) of insulin resistance, the role of neutrophils in this process has remained unclear until now.”

Neutrophils could be a new target for drugs developed to treat insulin resistance, say the scientists writing in the journal Nature Medicine. The enzyme secreted by neutrophils, called neutrophil elastase (NE), impairs insulin signalling. Removing NE from obese mice fed a high-fat diet improved their insulin sensitivity, the study showed.

“Given that NE mediates insulin resistance, one could, in theory, take an NE activity inhibitory approach to reverse or improve insulin resistance,” said Dr Oh.

  • 1 Comment

Readers' comments (1)

  • What could this mean for those on immunosuppressants who then develop type 2? Thank you,

    Unsuitable or offensive? Report this comment

Have your say

You must sign in to make a comment

Please remember that the submission of any material is governed by our Terms and Conditions and by submitting material you confirm your agreement to these Terms and Conditions. Links may be included in your comments but HTML is not permitted.