Abstract
In the past decade, islet inflammation has emerged as a contributor to the loss of functional β cell mass in both type 1 (T1D) and type 2 diabetes (T2D). Evidence supports the idea that overnutrition and insulin resistance result in the production of proinflammatory mediators by β cells. In addition to compromising β cell function and survival, cytokines may recruit macrophages into islets, thus augmenting inflammation. Limited but intriguing data imply a role of adaptive immune response in islet dysfunction in T2D. Clinical trials have validated anti-inflammatory therapies in T2D, whereas immune therapy for T1D remains challenging. Further research is required to improve our understanding of islet inflammatory pathways and to identify more effective therapeutic targets for T1D and T2D.
Copyright © 2013 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology
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Anti-Inflammatory Agents / therapeutic use
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Diabetes Mellitus, Type 1 / drug therapy
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Diabetes Mellitus, Type 1 / immunology*
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Diabetes Mellitus, Type 1 / metabolism
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Diabetes Mellitus, Type 2 / drug therapy
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Diabetes Mellitus, Type 2 / immunology*
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Diabetes Mellitus, Type 2 / metabolism
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Endoplasmic Reticulum Stress / drug effects
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Humans
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Hypoglycemic Agents / pharmacology
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Hypoglycemic Agents / therapeutic use
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Inflammation Mediators / metabolism*
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Insulin Resistance
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Islet Amyloid Polypeptide / metabolism
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Islets of Langerhans / drug effects
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Islets of Langerhans / immunology*
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Islets of Langerhans / metabolism
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Macrophages / drug effects
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Macrophages / immunology
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Macrophages / metabolism
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Molecular Targeted Therapy
Substances
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Anti-Inflammatory Agents
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Hypoglycemic Agents
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Inflammation Mediators
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Islet Amyloid Polypeptide