Targeting Inflammation in Diabetes through Disease-modifying Therapies

July 8, 2014
Jeannette Y. Wick, RPh, MBA, FASCP

An endocrinologist from the University Hospital Basel in Switzerland discusses the role of inflammation in the pathogenesis of type 2 diabetes, outlining the reasons why clinicians should target inflammation when treating diabetics.

In a review article published in Nature Reviews-Drug Discovery, an endocrinologist from the University Hospital Basel in Switzerland discussed the role of inflammation in the pathogenesis of type 2 diabetes, outlining the reasons why clinicians should target inflammation when treating diabetics.

Despite the availability of 8 classes of diabetes drugs, the review author, Marc Y. Donath, said diabetics have unmet needs in the greater context of inflammatory diseases such as rheumatoid arthritis (RA), gout, psoriatic arthritis (PsA), and Crohn’s disease (CD). Although the current drug classes treat diabetes symptoms, and some even delay the onset or progression of the disease, no current therapies offer the disease-modifying characteristics of the biologics used in other inflammatory conditions.

Donath contended that some of those anti-inflammatory treatments might be helpful in patients with diabetes, since therapies that address glycemia, prevent disease progression, target comorbidities, and have enduring benefits with minimal adverse effects are needed.

Donath reviewed the mechanisms of available biologics — such interleukin-1 (IL-1) receptor antagonism and tumor necrosis factor (TNF) inhibition — and their investigational use in diabetes. Of particular note, he discussed the anti-inflammatory properties of currently available diabetes drugs, though he noted that most have only marginal anti-inflammatory effects that are merely contributing mechanisms of actions.