Cell type-specific modulation of lipid mediator's formation in murine adipose tissue by omega-3 fatty acids
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
26707880
DOI
10.1016/j.bbrc.2015.12.055
PII: S0006-291X(15)31060-3
Knihovny.cz E-resources
- Keywords
- Adipose tissue macrophages, Lipid mediators, Lipidomics, Omega-3 PUFA, Protectin D1,
- MeSH
- Anti-Inflammatory Agents administration & dosage MeSH
- Administration, Oral MeSH
- Adipose Tissue, White cytology drug effects immunology MeSH
- Stromal Cells drug effects immunology MeSH
- Immunologic Factors immunology MeSH
- Cells, Cultured MeSH
- Macrophages cytology drug effects immunology MeSH
- Lipid Metabolism drug effects immunology MeSH
- Mice, Inbred C57BL MeSH
- Mice MeSH
- Fatty Acids, Omega-3 administration & dosage MeSH
- Dietary Supplements MeSH
- Adipocytes drug effects enzymology immunology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Anti-Inflammatory Agents MeSH
- Immunologic Factors MeSH
- Fatty Acids, Omega-3 MeSH
Mutual interactions between adipocytes and immune cells in white adipose tissue (WAT) are involved in modulation of lipid metabolism in the tissue and also in response to omega-3 polyunsaturated fatty acids (PUFA), which counteract adverse effects of obesity. This complex interplay depends in part on in situ formed anti- as well as pro-inflammatory lipid mediators, but cell types engaged in the synthesis of the specific mediators need to be better characterized. We used tissue fractionation and metabolipidomic analysis to identify cells producing lipid mediators in epididymal WAT of mice fed for 5 weeks obesogenic high-fat diet (lipid content 35% wt/wt), which was supplemented or not by omega-3 PUFA (4.3 mg eicosapentaenoic acid and 14.7 mg docosahexaenoic acid per g of diet). Our results demonstrate selective increase in levels of anti-inflammatory lipid mediators in WAT in response to omega-3, reflecting either their association with adipocytes (endocannabinoid-related N-docosahexaenoylethanolamine) or with stromal vascular cells (pro-resolving lipid mediator protectin D1). In parallel, tissue levels of obesity-associated pro-inflammatory endocannabinoids were suppressed. Moreover, we show that adipose tissue macrophages (ATMs), which could be isolated using magnetic force from the stromal vascular fraction, are not the major producers of protectin D1 and that omega-3 PUFA lowered lipid load in ATMs while promoting their less-inflammatory phenotype. Taken together, these results further document specific roles of various cell types in WAT in control of WAT inflammation and metabolism and they suggest that also other cells but ATMs are engaged in production of pro-resolving lipid mediators in response to omega-3 PUFA.
References provided by Crossref.org
Cardiac immune cell infiltration associates with abnormal lipid metabolism
