Islet Inflammation and β Cell Dysfunction in Type 2 Diabetes

Abstract

Pancreatic islets are the body’s central rheostat that regulates glucose homeostasis through the production of different hormones, including β cell-derived insulin. During obesity-induced type 2 diabetes (T2D), islet β cells become dysfunctional and inadequate insulin secretion no longer ensures glycemic control. T2D is associated with a chronic low-grade inflammation that manifests in several metabolic organs including the pancreatic islets. Growing evidence suggests that components of the innate immune system, and especially macrophages, play a crucial role in regulating islet homeostasis. Yet, the phenotypes and functions of islet macrophages in physiology and during T2D have only started to attract attention and remain unclear. In this review, the current knowledge about islet inflammation and macrophages will be summarized in humans and rodent models. Recent findings on the cellular and molecular mechanisms involved in islet remodeling and β cell function during obesity and T2D will be discussed.