Inflammatory stress in islet β-cells: therapeutic implications for type 2 diabetes?. (December 2018)

• Record Type: Journal Article
• Authors: Lytrivi, Maria; Igoillo-Esteve, Mariana; Cnop, Miriam
• Is Part Of: Current opinion in pharmacology. Volume 43(2018)
• Page Start: 40
• Page End: 45
• Publication Date: 2018-12
• Subjects: Pharmacology -- Periodicals; Pharmaceutical Preparations -- Periodicals; Drug Therapy -- Periodicals; Biopharmaceutics -- Periodicals; Pharmacologie -- Périodiques; Pharmacology; Periodicals; 615.105
• DOI: 10.1016/j.coph.2018.08.002
• Languages: English
• ISSNs: 1471-4892

Abstract

Highlights: Mild islet inflammation is present in type 2 diabetes. Potential triggers include excess nutrients, islet amyloid and humoral factors. Anti-inflammatory drugs are of modest efficacy in type 2 diabetes. The pathogenic role of islet inflammation remains unclear. Abstract : Type 2 diabetes is a common complex disease. Relatively little is known about the underlying pathophysiology. Mild islet inflammation has been suggested to play a pathogenic role; here we review the available evidence. Mild islet inflammation is histologically detected in pancreas sections of type 2 diabetic patients. In experimental models, it can be triggered by excess nutrients, amyloid, lipopolysaccharide, and endoplasmic reticulum and oxidative stress. Transcriptome studies do not consistently identify pro-inflammatory gene expression signatures in type 2 diabetic islets, and genetic evidence calls into question the causality of inflammation. Several anti-inflammatory medications confer a modest glucose-lowering effect, supporting the role for inflammation in type 2 diabetes. Whether these anti-inflammatory therapies target inflammation in islets or in other metabolically relevant tissues remains unknown.