| First Author | Turk J | Year | 2020 |
| Journal | Biomolecules | Volume | 10 |
| Issue | 10 | PubMed ID | 33080873 |
| Mgi Jnum | J:299007 | Mgi Id | MGI:6489633 |
| Doi | 10.3390/biom10101455 | Citation | Turk J, et al. (2020) Metabolic Effects of Selective Deletion of Group VIA Phospholipase A2 from Macrophages or Pancreatic Islet Beta-Cells. Biomolecules 10(10):1455 |
| abstractText | To examine the role of group VIA phospholipase A2 (iPLA2beta) in specific cell lineages in insulin secretion and insulin action, we prepared mice with a selective iPLA2beta deficiency in cells of myelomonocytic lineage, including macrophages (MO-iPLA2beta-KO), or in insulin-secreting beta-cells (beta-Cell-iPLA2beta-KO), respectively. MO-iPLA2beta-KO mice exhibited normal glucose tolerance when fed standard chow and better glucose tolerance than floxed-iPLA2beta control mice after consuming a high-fat diet (HFD). MO-iPLA2beta-KO mice exhibited normal glucose-stimulated insulin secretion (GSIS) in vivo and from isolated islets ex vivo compared to controls. Male MO-iPLA2beta-KO mice exhibited enhanced insulin responsivity vs. controls after a prolonged HFD. In contrast, beta-cell-iPLA2beta-KO mice exhibited impaired glucose tolerance when fed standard chow, and glucose tolerance deteriorated further when introduced to a HFD. beta-Cell-iPLA2beta-KO mice exhibited impaired GSIS in vivo and from isolated islets ex vivo vs. controls. beta-Cell-iPLA2beta-KO mice also exhibited an enhanced insulin responsivity compared to controls. These findings suggest that MO iPLA2beta 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, beta-cell iPLA2beta plays a role in GSIS and also appears to confer some protection against deterioration in beta-cell functions induced by a HFD. |
