Journal
CURRENT OPINION IN PHARMACOLOGY
Volume 43, Issue -, Pages 40-45Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2018.08.002
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Funding
- European Union's Horizon 2020 research and innovation programme, project T2DSystems [667191]
- Innovative Medicines Initiative 2 Joint Undertaking Rhapsody - European Union's Horizon 2020 research and innovation programme [115881]
- Swiss State Secretariat for Education Research and Innovation (SERI) [16.0097]
- competitive cluster Wagralim from Wallonia (FOOD4GUT project) [1318148]
- Fonds Erasme for medical research
- EFPIA
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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.
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