Reduced Number of Adipose Lineage and Endothelial Cells in Epididymal fat in Response to Omega-3 PUFA in Mice Fed High-Fat Diet
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články
Grantová podpora
16-05151S
Grantová Agentura České Republiky
LM2015062 Czech-BioImaging
Ministerstvo Školství, Mládeže a Tělovýchovy
PubMed
30567329
PubMed Central
PMC6316446
DOI
10.3390/md16120515
PII: md16120515
Knihovny.cz E-zdroje
- Klíčová slova
- adipocyte, cellularity, fat, nutrition, obesity, proliferation, white adipose tissue,
- MeSH
- bílá tuková tkáň účinky léků MeSH
- dieta s vysokým obsahem tuků MeSH
- endoteliální buňky účinky léků MeSH
- kyseliny mastné omega-3 aplikace a dávkování MeSH
- makrofágy účinky léků patologie MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- proliferace buněk účinky léků MeSH
- tukové buňky cytologie účinky léků MeSH
- zánět patologie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- kyseliny mastné omega-3 MeSH
We found previously that white adipose tissue (WAT) hyperplasia in obese mice was limited by dietary omega-3 polyunsaturated fatty acids (omega-3 PUFA). Here we aimed to characterize the underlying mechanism. C57BL/6N mice were fed a high-fat diet supplemented or not with omega-3 PUFA for one week or eight weeks; mice fed a standard chow diet were also used. In epididymal WAT (eWAT), DNA content was quantified, immunohistochemical analysis was used to reveal the size of adipocytes and macrophage content, and lipidomic analysis and a gene expression screen were performed to assess inflammatory status. The stromal-vascular fraction of eWAT, which contained most of the eWAT cells, except for adipocytes, was characterized using flow cytometry. Omega-3 PUFA supplementation limited the high-fat diet-induced increase in eWAT weight, cell number (DNA content), inflammation, and adipocyte growth. eWAT hyperplasia was compromised due to the limited increase in the number of preadipocytes and a decrease in the number of endothelial cells. The number of leukocytes and macrophages was unaffected, but a shift in macrophage polarization towards a less inflammatory phenotype was observed. Our results document that the counteraction of eWAT hyperplasia by omega-3 PUFA in dietary-obese mice reflects an effect on the number of adipose lineage and endothelial cells.
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