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Open AccessFeature PaperArticle

Metabolic Effects of Selective Deletion of Group VIA Phospholipase A2 from Macrophages or Pancreatic Islet Beta-Cells

1
Mass Spectrometry Facility, Division of Endocrinology, Metabolism, and Lipid Research, Department of Medicine, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA
2
Sigma-Aldrich Corporation, St. Louis, MO 63118, USA
3
Department of Cell, Developmental, and Integrative Biology, Comprehensive Diabetes Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA
*
Authors to whom correspondence should be addressed.
All three of these authors contributed equally to this manuscript and are co-primary authors.
Biomolecules 2020, 10(10), 1455; https://doi.org/10.3390/biom10101455
Received: 30 August 2020 / Revised: 8 October 2020 / Accepted: 13 October 2020 / Published: 17 October 2020
(This article belongs to the Special Issue Phospholipases: From Structure to Biological Function)
To examine the role of group VIA phospholipase A2 (iPLA2β) in specific cell lineages in insulin secretion and insulin action, we prepared mice with a selective iPLA2β deficiency in cells of myelomonocytic lineage, including macrophages (MØ-iPLA2β-KO), or in insulin-secreting β-cells (β-Cell-iPLA2β-KO), respectively. MØ-iPLA2β-KO mice exhibited normal glucose tolerance when fed standard chow and better glucose tolerance than floxed-iPLA2β control mice after consuming a high-fat diet (HFD). MØ-iPLA2β-KO mice exhibited normal glucose-stimulated insulin secretion (GSIS) in vivo and from isolated islets ex vivo compared to controls. Male MØ-iPLA2β-KO mice exhibited enhanced insulin responsivity vs. controls after a prolonged HFD. In contrast, β-cell-iPLA2β-KO mice exhibited impaired glucose tolerance when fed standard chow, and glucose tolerance deteriorated further when introduced to a HFD. β-Cell-iPLA2β-KO mice exhibited impaired GSIS in vivo and from isolated islets ex vivo vs. controls. β-Cell-iPLA2β-KO mice also exhibited an enhanced insulin responsivity compared to controls. These findings suggest that MØ iPLA2β participates in HFD-induced deterioration in glucose tolerance and that this mainly reflects an effect on insulin responsivity rather than on insulin secretion. In contrast, β-cell iPLA2β plays a role in GSIS and also appears to confer some protection against deterioration in β-cell functions induced by a HFD. View Full-Text
Keywords: pancreatic islets; β-cells; insulin secretion; glucose tolerance; insulin resistance; group VIA phospholipase A2 pancreatic islets; β-cells; insulin secretion; glucose tolerance; insulin resistance; group VIA phospholipase A2
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MDPI and ACS Style

Turk, J.; Song, H.; Wohltmann, M.; Frankfater, C.; Lei, X.; Ramanadham, S. Metabolic Effects of Selective Deletion of Group VIA Phospholipase A2 from Macrophages or Pancreatic Islet Beta-Cells. Biomolecules 2020, 10, 1455.

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