| First Author | Nascimento EBM | Year | 2018 |
| Journal | J Lipid Res | Volume | 59 |
| Issue | 2 | Pages | 273-282 |
| PubMed ID | 29233919 | Mgi Jnum | J:257479 |
| Mgi Id | MGI:6115164 | Doi | 10.1194/jlr.M079517 |
| Citation | Nascimento EBM, et al. (2018) Diacylglycerol kinase alpha deficiency alters inflammation markers in adipose tissue in response to a high-fat diet. J Lipid Res 59(2):273-282 |
| abstractText | Conversion of diacylglycerol to phosphatidic acid is mediated by diacylglycerol kinases (DGKs), with DGKalpha specifically linked to adaptive immune responses. We determined the role of DGKalpha in obesity and inflammatory responses to a high-fat diet (HFD). DGKalpha KO and WT littermates were either a) chow-fed, b) HFD-fed for 12 weeks (Long-Term HFD), or c) HFD-fed for 3 days (Acute HFD). Body weight/composition, oxygen consumption, food intake, and glucose tolerance was unaltered between chow-fed DGKalpha KO and WT mice. Insulin concentration during the intraperitoneal glucose tolerance (IPGT) test was elevated in chow-fed DGKalpha KO mice, suggesting mild insulin resistance. Insulin concentration during the IPGT test was reduced in Long-Term HFD-fed DGKalpha KO mice, suggesting a mild enhancement in insulin sensitivity. Acute HFD increased hormone sensitive lipase protein abundance and altered expression of interleukin 1beta mRNA, an inflammatory marker in perigonadal adipose tissue of DGKalpha KO mice. In conclusion, DGKalpha ablation is associated with mild alterations in insulin sensitivity. However, DGKalpha is dispensable for whole body insulin-mediated glucose uptake, hepatic glucose production, and energy homeostasis. Our results suggest DGKalpha aids in modulating the early immune response of adipose tissue following an acute exposure to HFD, possibly through modulation of acute T-cell action. |
