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Endoplasmic reticulum ER stress is becoming recognized as an important contributing factor in various diseases, including diabetes mellitus. The PLA 2 family of enzymes catalyse the hydrolysis of the sn -2 substituent i. Apoptosis can be mediated via an extrinsic death receptor or intrinsic mitochondrial pathway [ 18 lel, 19 ]. Recently, apoptosis as a result of prolonged endoplasmic reticulum ER stress has gained recognition [ 1820 — 22 ] and this process has been implicated as a causative factor in Alzheimer’s and Parkinson’s diseases and cancer [ 23 ].

Interruption of any of these functions can lead to production of malfolded proteins and their accumulation in the ER.

When an imbalance between the load of client proteins on the ER and the ER’s ability to process the load occurs, it results in ER stress [ 3536 ].

Prolonged ER stress promotes induction of stress factors and activation of caspase, localizedintheER [ 192137 ], andcansubsequently lead to downstream activation of caspase-3, a protease that is central to the execution of apoptosis [ 38 ]. The PLA 2 s are a diverse group of enzymes that catalyse the hydrolysis of the sn -2 substituent from glycerophospholipid substrates to yield a free fatty acid and a 2-lysophospholipid [ 40 ].

Arachidonic acid and its oxygenated metabolites are potent bioactive mediators that can regulate physiological and pathophysiological processes. These include ankyrin repeats, acyl-CoA esterase activity, caspase-3 cleavage consensus sequence, bipartite nuclear localization sequence and calmodulin-binding domain.

Ceramides are lipid messengers that can suppress cell growth and induce apoptosis [ 60 ] and they can be generated via multiple mechanisms de novo synthesis, sphingomyelin hydrolysis, inhibition of ceramide degradation or salvage pathway. While examining lipid profiles that might be associated with ER stress, we unexpectedly found a temporal increase in ceramides in the INS-1 cells [ 61 ].

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Ceramide accumulation has been linked to apoptosis through the intrinsic mitochondrial pathway. Although the ER- and mitochondria-associated apoptotic pathways can be activated independently, it has been suggested that induction of ER stress may lead to the triggering of intrinsic apoptotic processes [ 6263 ]. The authors would like to thank the expert technical assistance of Dr Mary Wohltmann and Mr Alan Bohrer for contributing to the work reviewed here. The authors do not declare any conflict of interest relevant to this manuscript.

National Center for Biotechnology InformationU. Author manuscript; available in PMC Jul Zhang1 B. Emani2 S. Barbour2 and S. Author information Copyright and License information Disclaimer. The publisher’s final edited version of this article is available at Diabetes Obes Metab. See other articles in PMC that cite the published article. Abstract Endoplasmic reticulum ER stress is becoming recognized as an important contributing factor in various diseases, including diabetes mellitus.

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Acknowledgements The authors would like to lwi the expert technical assistance of Dr Mary Wohltmann and Mr Alan Bohrer for contributing to the work reviewed here. Footnotes Conflict leii Interests The authors do not declare any conflict of interest relevant to lie manuscript.

Islet amyloid, increased A-cells, reduced B-cells and exocrine fibrosis: Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited. Surv Synth Pathol Res. Quantitation of endocrine cell content in the pancreas of nondiabetic and diabetic humans. J Clin Endocrinol Metab. Role of apoptosis in failure of beta-cell mass compensation for insulin resistance df beta-cell defects in the male Zucker diabetic fatty rat.

Induction of pancreatic islet neogenesis. Type 2 diabetes and beta cell apoptosis. Role of apoptosis in pancreatic beta-cell death in diabetes. Apoptosis in the beta cells: Beta-cell death during progression to diabetes. Nitric oxide-induced apoptosis in pancreatic beta cells is mediated by the endoplasmic reticulum stress pathway. Caspases find a new place to hide. Bitko V, Barik S. An endoplasmic reticulum-specific stress-activated caspase caspase is implicated in the apoptosis of A epithelial cells by respiratory syncytial virus.

Caspase mediates endoplasmicreticulum-specific apoptosis and cytotoxicity by amyloid-beta.

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Coupling endoplasmic reticulum stress to the cell death program. An Apafindependent intrinsic pathway. Hosoi T, Ozawa K. Endoplasmic reticulum stress in disease: Endoplasmic reticulum stress-mediated apoptosis in pancreatic beta-cells.

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Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes. The role of endoplasmic reticulum stress in nonimmune diabetes: Ann N Y Acad Sci. EIF2AK3, encoding translation initiation factor 2-alpha kinase 3, se mutated in patients with Wolcott-Rallison syndrome.

WFS1 Wolfram syndrome 1 gene product: Endoplasmic reticulum stress and diabetes mellitus.

Aridor M, Balch 10158. Integration of endoplasmic reticulum signaling in health and disease. Translational control in the endoplasmic reticulum stress response. Harding HP, Ron D.

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Endoplasmic reticulum stress and the development of diabetes: Semin Cell Dev Biol. Quantitative distribution of phospholipids in neurons and glial cells isolated from rat cerebral cortex. Mass spectrometric characterization of arachidonate-containing plasmalogens in human pancreatic islets and in rat islet beta-cells and subcellular membranes. Mass spectrometric identification and quantitation of arachidonate-containing phospholipids in pancreatic islets: The phospholipase A 2 superfamily and its group numbering system.

Turk J, Ramanadham S. Can J Physiol Pharmacol. Regulation of group VIA phospholipase A 2 expression by sterol availability. Rat and human pancreatic islet cells contain a calcium ion independent phospholipase A 2 activity selective for hydrolysis of arachidonate which is stimulated by adenosine triphosphate and is specifically localized to islet beta-cells. Inhibition of arachidonate release by secretagogue-stimulated pancreatic islets suppresses both insulin secretion and the rise in beta-cell cytosolic calcium ion concentration.

Studies of the role of group vi phospholipase A 2 in fatty acid incorporation, phospholipid remodeling, lysophosphatidylcholine generation, and secretagogue-induced arachidonic acid release in pancreatic islets and insulinoma cells. Apoptosis in insulin-secreting cells. Distinct roles of two intracellular phospholipase A 2 s in fatty acid release in the cell death pathway. The Group VIA calcium-independent phospholipase A 2 participates in ER stress-induced INS-1 insulinoma cell apoptosis by promoting ceramide generation via hydrolysis of sphingomyelins by neutral sphingomyelinase.

Kayo T, Koizumi A. Mapping of murine diabetogenic gene mody on chromosome 7 at D7Mit and its involvement in pancreatic islet and beta cell development during the perinatal period. J Physiol Lond ; Am J Physiol Endocrinol Metab. Activation of neutral sphingomyelinase in human neutrophils by polyunsaturated fatty acids. Kim JB, Spiegelman B. Support Center Support Center. Please review our privacy policy.