Islet inflammation in type 2 diabetes and physiology
Kosei Eguchi, Ryozo Nagai
Kosei Eguchi, Ryozo Nagai
Published January 3, 2017
Citation Information: J Clin Invest. 2017;127(1):14-23. https://doi.org/10.1172/JCI88877.
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Review Series

Islet inflammation in type 2 diabetes and physiology

Abstract

The finding of islet inflammation in type 2 diabetes (T2D) and its involvement in β cell dysfunction has further highlighted the significance of inflammation in metabolic diseases. The number of intra-islet macrophages is increased in T2D, and these cells are the main source of proinflammatory cytokines within islets. Multiple human studies of T2D have shown that targeting islet inflammation has the potential to be an effective therapeutic strategy. In this Review we provide an overview of the cellular and molecular mechanisms by which islet inflammation develops and causes β cell dysfunction. We also emphasize the regulation and roles of macrophage polarity shift within islets in the context of T2D pathology and β cell health, which may have broad translational implications for therapeutics aimed at improving islet function.

Authors

Kosei Eguchi, Ryozo Nagai

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Figure 1

M1-like polarization of islet macrophages plays important roles in islet inflammation and β cell dysfunction in T2D.

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M1-like polarization of islet macrophages plays important roles in islet...
The communication between islet macrophages and β cells via hIAPP, chemokines (e.g., CCL2 and CXCL1), and proinflammatory cytokines (e.g., IL-1β) initiate and amplify the M1-like polarity shift of islet macrophages and islet inflammation. The inflammasome/IL-1β pathway in islet macrophages is a common pathway that causes β cell dysfunction within inflamed islets in T2D.