Reduced Number of Adipose Lineage and Endothelial Cells in Epididymal fat in Response to Omega-3 PUFA in Mice Fed High-Fat Diet.
Katerina AdamcovaOlga HorakovaKristina BardovaPetra JanovskaMarie BrezinovaOndřej KudaMartin RossmeislJan KopeckyPublished in: Marine drugs (2018)
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.
Keyphrases
- adipose tissue
- high fat diet
- insulin resistance
- high fat diet induced
- endothelial cells
- metabolic syndrome
- gene expression
- skeletal muscle
- single cell
- flow cytometry
- oxidative stress
- induced apoptosis
- type diabetes
- high glucose
- weight loss
- bone marrow
- dna methylation
- randomized controlled trial
- high throughput
- body mass index
- genome wide
- cell proliferation
- clinical trial
- signaling pathway
- body weight
- cell death
- vascular endothelial growth factor
- gestational age
- cell fate
- data analysis
- endoplasmic reticulum stress
- study protocol