Inflammation and the etiology of type 2 diabetes
Article first published online: 1 JUL 2005
Copyright © 2005 John Wiley & Sons, Ltd.
Diabetes/Metabolism Research and Reviews
Volume 22, Issue 1, pages 4–10, January/February 2006
How to Cite
Sjöholm, Å. and Nyström, T. (2006), Inflammation and the etiology of type 2 diabetes. Diabetes Metab. Res. Rev., 22: 4–10. doi: 10.1002/dmrr.568
- Issue published online: 17 DEC 2005
- Article first published online: 1 JUL 2005
- Manuscript Accepted: 11 MAY 2005
- Manuscript Revised: 8 DEC 2004
- Manuscript Received: 3 SEP 2004
Type 2 diabetes is increasingly common worldwide and is beginning to strike younger age groups. Almost 90% of all patients with diabetes show insulin resistance, which also precedes the first symptoms of diabetes. The mechanisms underlying the development of insulin resistance are not well understood. In recent years, several studies have been published that implicate subclinical chronic inflammation as an important pathogenetic factor in the development of insulin resistance and type 2 diabetes. This opens new perspectives for diagnosis and treatment of early insulin resistance and incipient glucose intolerance.
Surrogate markers for this low-grade chronic inflammation include CRP, IL-6 and TNF-α. Some antidiabetic agents, for example, glitazones that reduce insulin resistance, and insulin itself, reduce inflammation. Conversely, antiinflammatory drugs (ASA/NSAID) may improve glucose tolerance. Vasoactive drugs that are often prescribed to people with diabetes, for example, statins and ACE inhibitors/angiotensin receptor antagonists, also counteract inflammation and reduce the risk of type 2 diabetes. More specific and sensitive biomarkers should be identified, which may predict early disturbances in insulin sensitivity and cardiovascular risk. Also, inflammatory signalling pathways need to be explored in greater detail, and may form the basis of drugable targets against the epidemic of insulin resistance and atherosclerosis. Copyright © 2005 John Wiley & Sons, Ltd.