Ablation of eNOS does not promote adipose tissue inflammation

作者：Jurrissen Thomas J; Sheldon Ryan D; Gastecki Michelle L; Woodford Makenzie L; Zidon Terese M; Rector R Scott; Vieira Potter Victoria J; Padilla Jaume^*

来源：American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, 2016, 310(8): R744-R751.

DOI：10.1152/ajpregu.00473.2015

• obesity
• Western diet
• adipose tissue
• endothelial nitric oxide synthase

Ablation of eNOS does not promote adipose tissue inflammation. Am J Physiol Regul lntegr Comp Physiol 310: R744 R751, 2016. First published February 10, 2016; doi:10.1152/4regu.00473.2015. Adipose tissue (AT) inflatrimation 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) bioavai.lability promotes arterial.inflamm.ation; however, the role of NO in modulating inflammation in AT remains disputed. In the present study, 10-wk-old C57BL6 wild-type and endothelial nitric oxide synthase (eNOS) knockout male mice were randomized to either a control diet (10% kcal from fat) or a Western diet (44.9% kcal from fat, 17% sucrose, and 1% cholesterol) for 18 wk In = 7 or 8/group). In wild-type mice, Western diet -induced obesity led to increased visceral white Al' expression of inflammatory genes (e.g., M('Pl, 'INF-alpha, and C(71,5 mRNAs) and markers of macrophage infiltration (e.g., CD68, ITGAM, EMRE CD11C mRNAs, and Mac -2 protein), as well as reduced markers of mitochondrial content (e.g., OXPHC)S complex I and IV protein). Unexpectedly, these effects of Western diet on visceral white AT were not accompanied by decreases in eNOS phosphorylation at Ser-1177 or increases in eNOS phosphorylation at Thr-495. Also counter to expectations, eNOS knockout mice, independent of the diet, were leaner and did not exhibit greater white or brown AT inflanunation compared with wild-type mice. Collectively, these findings do not support the hypothesis that reduced NC) production from eNOS contributes to obesity-related AT inflammation

• 出版日期2016-4-15