Islet inflammation in type 2 diabetes

Excerpt

The term inflammation originates from the Latin, inflammatio, meaning ‘setting on fire’, and in medicine it indicates the reaction of tissues to injuries induced by different causes. Classically, inflammation is a protective response, which involves many complex signals and aims to repair tissue and restore homeostasis [1]. However, dysregulated or prolonged inflammation states have been associated with many diseases, including type 2 diabetes [1]. Early connections between inflammation, obesity and type 2 diabetes were made in the 1990s, in both rodent models and humans [2, 3], and later substantiated by a large body of evidence (see [4‐7] for recent reviews). Then, it was observed that pancreatic islet cells may also show signs of inflammation, including immune cell infiltration [8‐10] and increased expression of cytokines and chemokines [11‐13]. It has been shown that a proinflammatory milieu can lead to reduced beta cell function and survival [14‐16]. Given the key role of beta cell impairment in the onset and progression of diabetes [17, 18], it is of utmost importance to shed light on the several features linking inflammation and islet cell dysfunction. This commentary on the ‘Islet inflammation in type 2 diabetes’ symposium at the EASD 2015 meeting focuses on a few general issues regarding the association between inflammation and the pancreatic islets in human type 2 diabetes. It is accompanied by articles that specifically address the mechanistic implications [19, 20] and therapeutic perspectives [21]. …