NDLI: Diminished acyl-CoA synthetase isoform 4 activity in INS 832/13 cells reduces cellular epoxyeicosatrienoic acid levels and results in impaired glucose-stimulated insulin secretion.

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Diminished acyl-CoA synthetase isoform 4 activity in INS 832/13 cells reduces cellular epoxyeicosatrienoic acid levels and results in impaired glucose-stimulated insulin secretion.

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Diminished acyl-CoA synthetase isoform 4 activity in INS 832/13 cells reduces cellular epoxyeicosatrienoic acid levels and results in impaired glucose-stimulated insulin secretion.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Klett, Eric L. Edin, Matthew L. Ilkayeva, Olga Chen, Shufen Coleman, Rosalind A. Li, Lei O. Newgard, Christopher B. Zeldin, Darryl C.
Description	Author Affiliation: Klett EL ( Department of Medicine, Division of Endocrinology, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7172, USA. eklett@med.unc.edu)
Abstract	Glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells is potentiated by fatty acids (FA). The initial step in the metabolism of intracellular FA is the conversion to acyl-CoA by long chain acyl-CoA synthetases (Acsls). Because the predominantly expressed Acsl isoforms in INS 832/13 cells are Acsl4 and -5, we characterized the role of these Acsls in beta-cell function by using siRNA to knock down Acsl4 or Acsl5. Compared with control cells, an 80% suppression of Acsl4 decreased GSIS and FA-potentiated GSIS by 32 and 54%, respectively. Knockdown of Acsl5 did not alter GSIS. Acsl4 knockdown did not alter FA oxidation or long chain acyl-CoA levels. With Acsl4 knockdown, incubation with 17 mm glucose increased media epoxyeicosatrienoic acids (EETs) and reduced cell membrane levels of EETs. Further, exogenous EETs reduced GSIS in INS 832/13 cells, and in Acsl4 knockdown cells, an EET receptor antagonist partially rescued GSIS. These results strongly suggest that Acsl4 activates EETs to form EET-CoAs that are incorporated into glycerophospholipids, thereby sequestering EETs. Exposing INS 832/13 cells to arachidonate or linoleate reduced Acsl4 mRNA and protein expression and reduced GSIS. These data indicate that Acsl4 modulates GSIS by regulating the levels of unesterified EETs and that arachidonate controls the expression of its activator Acsl4.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	30
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-07-26
Publisher Place	United States
Access Restriction	Open
Subject Keyword	8,11,14-Eicosatrienoic Acid Analogs & Derivatives Coenzyme A Ligases Metabolism Glucose Pharmacology Insulin-Secreting Cells Drug Effects Insulin Secretion Acyl Coenzyme A Animals Blotting, Western Cell Line, Tumor Genetics Fatty Acids Gene Expression Regulation, Neoplastic Glycerophospholipids Pathology Insulinoma Membrane Lipids Mitochondrial Proteins Oxidation-Reduction RNA Interference Reverse Transcriptase Polymerase Chain Reaction Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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