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Ablation of eNOS Does Not Promote Adipose Tissue Inflammation
Author(s) -
Jurrissen Thomas J,
Sheldon Ryan D,
Gastecki Michelle L,
Zidon Terese M,
Rector R. Scott,
VieiraPotter Victoria J,
Padilla Jaume
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1292.4
Subject(s) - inflammation , enos , endocrinology , medicine , adipose tissue , white adipose tissue , knockout mouse , overweight , obesity , nitric oxide , biology , nitric oxide synthase , receptor
Adipose tissue (AT) inflammation is a hallmark characteristic of obesity and an important determinant of insulin resistance and cardiovascular disease; therefore, a better understanding of factors regulating AT inflammation is critical. It is well established that reduced vascular endothelial nitric oxide (NO) bioavailability promotes arterial inflammation; however, the role of NO in modulating inflammation in AT remains disputed. In the present study, ten‐week old C57BL6 wild‐type and eNOS knockout male mice were randomized to either a control diet (10% kcal from fat) or Western diet (45% kcal from fat, 17% sucrose, and 1% cholesterol) for 18 weeks (n=7–8/group). In wild‐type mice, Western diet‐induced obesity led to increased visceral white AT expression of inflammatory genes (e.g., MCP1, TNFα, CCL5 mRNAs) and markers of macrophage infiltration (e.g., CD68, ITGAM, EMR1, CD11C mRNAs and Mac‐2 protein), as well as reduced markers of mitochondrial content (e.g., oxphos complex I and IV protein). These effects of Western diet on visceral white AT were not accompanied by decreases in eNOS activation. eNOS knockout mice, independent of the diet, were leaner and did not exhibit greater white or brown AT inflammation compared to wild‐type mice. Collectively, these findings do not support the hypothesis that reduced NO signaling contributes to obesity‐related AT inflammation. Support or Funding Information This work was supported by a University of Missouri Life Sciences Fellowship (R. D. Sheldon), Veterans Health Administration grant CDA2 BX001299 (R. S. Rector), and National Institute of Health grants K01 HL‐125503 and R21 DK‐105368 (J. Padilla).