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Blunting of Endothelium Dependent Dilation in Adipose Tissue Arteries by Tumor Necrosis Factor Alpha is Lost after High Fat Feeding
Author(s) -
McCullagh Joseph P,
Henson Grant D.,
Donato Anthony J.,
Lesniewski Lisa A.
Publication year - 2012
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.26.1_supplement.680.17
Subject(s) - medicine , endocrinology , adipose tissue , endothelium , endothelial dysfunction , sodium nitroprusside , white adipose tissue , insulin resistance , tumor necrosis factor alpha , vasodilation , obesity , chemistry , nitric oxide
Tumor necrosis factor alpha (TNF) is implicated in metabolic and endothelial dysfunction with obesity and aging. Although adipose tissue blood flow is reduced with obesity, the cause and consequences on lipid handling and systemic insulin sensitivity are not known. Impaired endothelial function in the resistance arteries of the white adipose tissue (WAT) per se may play a role. We determined if TNF impairs endothelium dependent dilation (EDD) in WAT resistance arteries of young normal chow (Y NC: 4–7 mo) fed mice and if this effect is lost in arteries from Y high fat (Y HF: 8–10 weeks) and old (O NC: 28–31 mo) fed B6D2F1 mice. Maximal EDD to acetylcholine was lower in WAT arteries from both Y HF (68 ± 8%, P<0.01) and O NC (82 ± 6%, P<0.01) vs Y NC mice (95 ± 2%). Recombinant TNF (1 ng/ml, 60 min) reduced EDD in WAT arteries from Y (69 ± 10%, P<0.01) and O NC (47 ± 4%, P<0.01), but not Y HF (65 ± 0.1%) mice. Endothelium independent dilation to sodium nitroprusside did not differ between groups (ALL P>0.05). Compared to Y NC (9.4 ± 1.1 pg/ml), WAT TNF concentration was increased in Y HF (17 ± 3, P<0.01) but not in O NC (11 ± 2) mice. Although these results suggest that previous exposure to excessive TNF in vivo may be responsible for impaired EDD in WAT arteries after HF feeding but not aging, it remains to be determined if endothelial dysfunction in WAT arteries contributes to diminished WAT blood flow and subsequently to inappropriate lipid storage and systemic metabolic/vascular derangements. Support: NIA‐ AG033196 , NIA‐ AG033755