Eicosanoids, β-cell function, and diabetes

Luo, Pengfei; Wang, Mong Heng

doi:10.1016/j.prostaglandins.2011.06.001

Cited by 94 publications

(107 citation statements)

References 168 publications

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“…This is consistent with the reports that in contrast to the islets, which are enriched in AA-containing glycerophospholipids, the most prominent sn -2 substituent in brain glycerophospholipids is DHA ( 297,298 ), and iPLA 2 ␤ -defi ciency results in reduced DHA metabolism and content in the brain ( 299 ). Considering generate eicosanoids ( 97,125,245,264 ). These bioactive lipids act as paracrine and autocrine factors and greatly contribute to infl ammation (264)(265)(266) and autoimmune diseases (267)(268)(269)(270)(271)(272)(273)(274).…”

Section: Ipla 2 ␤ and Diseasessupporting

confidence: 89%

“…Considering generate eicosanoids ( 97,125,245,264 ). These bioactive lipids act as paracrine and autocrine factors and greatly contribute to infl ammation (264)(265)(266) and autoimmune diseases (267)(268)(269)(270)(271)(272)(273)(274). PGE 2 has been reported to reduce debris clearance ( 275 ), and apoptotic clearance defects in non-obese diabetic (NOD) macrophages and dendritic cells are attributed to high PGE 2 levels ( 276,277 ).…”

Section: Ipla 2 ␤ and Diseasesmentioning

confidence: 99%

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Calcium-independent phospholipases A2 and their roles in biological processes and diseases

Ramanadham

Ali

Ashley

et al. 2015

Journal of Lipid Research

167

190

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The Ca 2+ -independent phospholipases A 2 (iPLA 2 s) are part of a diverse family of PLA 2 s that hydrolyze the sn -2 substituent from membrane phospholipids to release a free fatty acid and a lysolipid ( 1, 2 ). These enzymes are ubiquitously expressed, and in contrast to secretory PLA 2 s (sPLA 2 s) and cytosolic PLA 2 s (cPLA 2 s), do not require Ca 2+ for either translocation or activity. Some of the fi rst descriptions of iPLA 2 activity were in the mid-to late-1980s with the identifi cation of a plasmalogen-selective PLA 2 in Abstract Among the family of phospholipases A 2 (PLA 2 s) are the Ca 2+ -independent PLA 2 s (iPLA 2 s) and they are designated group VI iPLA 2 s. In relation to secretory and cytosolic PLA 2 s, the iPLA 2 s are more recently described and details of their expression and roles in biological functions are rapidly emerging. The iPLA 2 s or patatin-like phospholipases (PNPLAs) are intracellular enzymes that do not require Ca 2+ for activity, and contain lipase (GXSXG) and nucleotide-binding (GXGXXG) consensus sequences. Though nine PNPLAs have been recognized, PNPLA8 (membraneassociated iPLA 2 ␥ ) and PNPLA9 (cytosol-associated iPLA 2 ␤ ) are the most widely studied and understood. The iPLA 2 s manifest a variety of activities in addition to phospholipase, are ubiquitously expressed, and participate in a multitude of biological processes, including fat catabolism, cell differentiation, maintenance of mitochondrial integrity, phospholipid remodeling, cell proliferation, signal transduction, and cell death. As might be expected, increased or decreased expression of iPLA 2 s can have profound effects on the metabolic state, CNS function, cardiovascular performance, and cell survival; therefore, dysregulation of iPLA 2 s can be a critical factor in the development of many diseases. This review is aimed at providing a general framework of the current understanding of the iPLA 2 s and discussion of the potential mechanisms of action of the iPLA 2 s and related involved lipid mediators. -Ramanadham, S

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Section: Ipla 2 ␤ and Diseasessupporting

confidence: 89%

Section: Ipla 2 ␤ and Diseasesmentioning

confidence: 99%

Calcium-independent phospholipases A2 and their roles in biological processes and diseases

Ramanadham

Ali

Ashley

et al. 2015

Journal of Lipid Research

167

190

View full text Add to dashboard Cite

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“…Previous studies have shown that arachidonic acid (AA) and linoleic acid (LA) and their metabolites are involved in the regulation of beta cell function [12]. We have shown in INS-1E cells that high glucose levels induced remodelling of membrane phospholipids and released AA and LA.…”

Section: Introductionmentioning

confidence: 84%

“…Previous findings demonstrating the protective role of oleic acid in PAtreated beta cells [34] could be explained by the replenishment of the former when SCD1 predominately transforms PA to palmitoleic acid. PUFA are transformed by cyclooxygenases, lipoxygenases and cytochrome P 450 epoxidase/ω-hydrolase to a large number of mediators, which regulate various beta cell functions [12,35,36]. The increased cyclooxygenase-mediated production of PGE 2 in PA-treated cells (ESM Fig.…”

Section: Discussionmentioning

confidence: 99%

Beta cell response to nutrient overload involves phospholipid remodelling and lipid peroxidation

et al. 2015

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Aims/hypothesis Membrane phospholipids are the major intracellular source for fatty acid-derived mediators, which regulate myriad cell functions. We showed previously that high glucose levels triggered the hydrolysis of polyunsaturated fatty acids from beta cell phospholipids. These fatty acids were subjected to free radical-catalysed peroxidation to generate the bioactive aldehyde 4-hydroxy-2E-nonenal (4-HNE). The latter activated the nuclear peroxisome proliferator-activated receptor-δ (PPARδ), which in turn augmented glucosestimulated insulin secretion. The present study aimed at investigating the combined effects of glucose and fatty acid overload on phospholipid turnover and the subsequent generation of lipid mediators, which affect insulin secretion and beta cell viability. Methods INS-1E cells were incubated with increasing glucose concentrations (5-25 mmol/l) without or with palmitic acid (PA; 50-500 μmol/l) and taken for fatty acid-based lipidomic analysis and functional assays. Rat isolated islets of Langerhans were used similarly. Results PA was incorporated into membrane phospholipids in a concentration-and time-dependent manner; incorporation was highest at 25 mmol/l glucose. This was coupled to a rapid exchange with saturated, mono-unsaturated and polyunsaturated fatty acids. Importantly, released arachidonic acid and linoleic acid were subjected to peroxidation, resulting in the generation of 4-HNE, which further augmented insulin secretion by activating PPARδ in beta cells. However, this adaptive increase in insulin secretion was abolished at high glucose and PA levels, which induced endoplasmic reticulum stress, apoptosis and cell death. Conclusions/interpretation These findings highlight a key role for phospholipid remodelling and fatty acid peroxidation in mediating adaptive and cytotoxic interactions induced by nutrient overload in beta cells.

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“…Several studies have shown that the disruption of sEH enhanced islet glucose-stimulated insulin secretion through AMPK signaling and decreased islet cell apoptosis in diabetes (2,20,54). Genetic disruption or pharmacologic inhibition of sEH prevents hyperglycemia in a T1D model induced by streptozotocin administration.…”

Section: Diabetesmentioning

confidence: 99%

The Role of Cytochrome P450 Epoxygenases, Soluble Epoxide Hydrolase, and Epoxyeicosatrienoic Acids in Metabolic Diseases

Chen

et al. 2016

Advances in Nutrition

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Metabolic diseases are associated with an increased risk of developing cardiovascular disease. The features comprising metabolic diseases include obesity, insulin resistance, hyperglycemia, hyperlipidemia, and hypertension. Recent evidence has emerged showcasing a role for cytochrome P450 epoxygenases, soluble epoxide hydrolase, and epoxyeicosatrienoic acids (EETs) in the development and progression of metabolic diseases. This review discusses the current knowledge related to the modulation of cytochrome P450 epoxygenases and soluble epoxide hydrolase to alter concentrations of biologically active EETs, resulting in effects on insulin resistance, lipid metabolism, obesity, and diabetes. Future areas of research to address current deficiencies in the understanding of these enzymes and their eicosanoid metabolites in various aspects of metabolic diseases are also discussed. Adv Nutr 2016;7:1122-8.

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Eicosanoids, β-cell function, and diabetes

Cited by 94 publications

References 168 publications

Calcium-independent phospholipases A2 and their roles in biological processes and diseases

Calcium-independent phospholipases A2 and their roles in biological processes and diseases

Beta cell response to nutrient overload involves phospholipid remodelling and lipid peroxidation

The Role of Cytochrome P450 Epoxygenases, Soluble Epoxide Hydrolase, and Epoxyeicosatrienoic Acids in Metabolic Diseases

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