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dc.creatorCnop, M.-
dc.creatorLadrière, L.-
dc.creatorIgoillo‐Esteve, M.-
dc.creatorMoura, R. F.-
dc.creatorCunha, D. A.-
dc.identifier.citationCNOP, N. et al. Causes and cures for endoplasmic reticulum stress in lipotoxic β‐cell dysfunction. Diabetes, Obesity and Metabolism: A Journal of Pharmacology and Therapeutics, [S. l.], v. 12, n. s2, p. 76-82, Oct. 2010. Special Issue.pt_BR
dc.description.abstractPancreatic β‐cell dysfunction is central to the pathogenesis of type 2 diabetes, and the loss of functional β‐cell mass in type 2 diabetes is at least in part secondary to increased β‐cell apoptosis. Accumulating evidence suggests that endoplasmic reticulum (ER) stress is present in β‐cells in type 2 diabetes. Free fatty acids (FFAs) cause ER stress and are putative mediators of β‐cell dysfunction and death. In this review, we discuss the molecular mechanisms underlying ER stress induced by saturated and unsaturated FFAs. Oleate and palmitate trigger ER stress through ER Ca2+ depletion and build‐up of unfolded proteins in the secretory pathway. Saturated and unsaturated FFAs elicit a differential signal transduction in the three branches of the ER stress response, resulting in different survival/apoptosis outcomes. The protection of β‐cells against FFAs through the interference with ER stress signalling has opened novel therapeutic perspectives for type 2 diabetes. Chemical chaperones, salubrinal and glucagon‐like peptide‐1 (GLP‐1) analogues have been used to protect β‐cells from lipotoxic ER stress. Importantly, the pro‐ and antiapoptotic effects of these compounds are cell and context dependent.pt_BR
dc.sourceDiabetes, Obesity and Metabolism: A Journal of Pharmacology and Therapeuticspt_BR
dc.subjectEndoplasmic reticulum stresspt_BR
dc.subjectFree fatty acidspt_BR
dc.subjectPancreatic β‐cellspt_BR
dc.subjectUnfolded protein responsept_BR
dc.subjectTensão do retículo endoplasmáticopt_BR
dc.subjectÁcidos graxos livrespt_BR
dc.subjectResposta da proteína desdobradapt_BR
dc.titleCauses and cures for endoplasmic reticulum stress in lipotoxic β‐cell dysfunctionpt_BR
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