title: Endoplasmic reticulum stress, obesity and diabetes.
abstract: The endoplasmic reticulum (ER) stress response, also commonly known as the unfolded protein response (UPR), is an adaptive response used to align ER functional capacity with demand. It is activated in various tissues under conditions related to obesity and type 2 diabetes. Hypothalamic ER stress contributes to inflammation and leptin/insulin resistance. Hepatic ER stress contributes to the development of steatosis and insulin resistance, and components of the UPR regulate liver lipid metabolism. ER stress in enlarged fat tissues induces inflammation and modifies adipokine secretion, and saturated fats cause ER stress in muscle. Finally, prolonged ER stress impairs insulin synthesis and causes pancreatic β cell apoptosis. In this review, we discuss ways in which ER stress operates as a common molecular pathway in the pathogenesis of obesity and diabetes.
authors: Laboratory of Experimental Medicine, Université Libre de Bruxelles (ULB), CP-618, Route de Lennik 808, 1070 Brussels, Belgium. mcnop@ulb.ac.be
authors: Miriam
authors: M
authors: Cnop
authors: Fabienne
authors: F
authors: Foufelle
authors: Licio A
authors: LA
authors: Velloso
mesh_terms: D000818:Animals; D003920:Diabetes Mellitus / Q000378:metabolism*; D059865:Endoplasmic Reticulum Stress; D006801:Humans; D009765:Obesity / Q000378:metabolism*; D015398:Signal Transduction