Preserving insulin secretion in Type 2 diabetes mellitus

Abstract

Type 2 diabetes mellitus (T2DM) is a complex disease characterized by insulin resistance and a progressive decline in β-cell function and mass. Current evidence suggests that β-cell dysfunction is present early in the course of the disease and that this dysfunction, rather than insulin resistance, is primarily responsible for the progression of T2DM. β-cell dysfunction can be accelerated by glucose toxicity, lipotoxicity, oxidative stress, chronic increases in inflammatory mediators and, potentially, the use of sulfonylureas. This review suggests that future efforts to limit the impact of T2DM must focus on strategies to preserve β-cell function. Several interventions have shown promise in this regard, including lifestyle modifications, thiazolidinediones, potassium channel openers, incretin mimetics, cytokine antagonists, bariatric surgery and dipeptidyl peptidase IV inhibitors, although therapeutic insulin remains the most robust and physiological approach.

Keywords::

• β-cell function
• bariatric surgery
• cytokine antagonists
• diabetes mellitus
• dipeptidyl peptidase IV inhibitors
• incretin mimetics
• insulin
• insulin resistance
• insulin secretion
• potassium channel openers
• thiazolidinediones
• Type 2 diabetes

Financial & competing interests disclosure

J Tibaldi serves as a consultant for Novo Nordisk and is on speakers bureaus for GlaxoSmithKline, Merck, Novartis, Novo Nordisk, and sanofi-aventis. The author wishes to thank Novo Nordisk for funding that helped support preparation of this manuscript. The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Writing assistance was utilized in the production of this manuscript. Kathryn J Lucchesi and Nicole Cooper provided writing and editorial support.

Notes

From [9].