Full text

Turn on search term navigation

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

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.

Details

Title
Metabolic Effects of Selective Deletion of Group VIA Phospholipase A2 from Macrophages or Pancreatic Islet Beta-Cells
Author
Turk, John 1 ; Song, Haowei 2 ; Wohltmann, Mary 1 ; Frankfater, Cheryl 1 ; Lei, Xiaoyong 3 ; Ramanadham, Sasanka 3 

 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; [email protected] (H.S.); [email protected] (M.W.); [email protected] (C.F.) 
 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; [email protected] (H.S.); [email protected] (M.W.); [email protected] (C.F.); Sigma-Aldrich Corporation, St. Louis, MO 63118, USA 
 Department of Cell, Developmental, and Integrative Biology, Comprehensive Diabetes Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA; [email protected] 
First page
1455
Publication year
2020
Publication date
2020
Publisher
MDPI AG
e-ISSN
2218273X
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2547481990
Copyright
© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.