@article{lytrivi_inflammatory_2018, title = {Inflammatory stress in islet β-cells: therapeutic implications for type 2 diabetes?}, volume = {43}, issn = {1471-4973}, shorttitle = {Inflammatory stress in islet β-cells}, doi = {10.1016/j.coph.2018.08.002}, 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.}, language = {eng}, journal = {Current Opinion in Pharmacology}, author = {Lytrivi, Maria and Igoillo-Esteve, Mariana and Cnop, Miriam}, month = dec, year = {2018}, pmid = {30142486}, keywords = {WP5}, pages = {40--45}, }