<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Canavan, Neil</style></author></authors><secondary-authors><author><style face="normal" font="default" size="100%">Eizirik, D.L.</style></author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">ER Stress Induces Beta-Cell Apoptosis</style></title><secondary-title><style face="normal" font="default" size="100%">MD Conference Express</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008-10-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">29-30</style></pages><abstract><style  face="normal" font="default" size="100%">A growing consensus links the loss of beta-cell mass with the development of type 2 diabetes mellitus. This article demonstrates that endoplasmic reticulum stress, induced by high levels of saturated free fatty acids, triggers a response that leads to eventual beta-cell apoptosis. This observation suggests one or more new targets for the therapeutic maintenance of beta-cell populations.</style></abstract><number><style face="normal" font="default" size="100%">7</style></number><volume><style face="normal" font="default" size="100%">8</style></volume></record></records></xml>