{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T01:32:00Z","timestamp":1791250320789,"version":"4.1.0"},"reference-count":44,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2012,9,15]]},"abstract":"<jats:p>\n                    We tested the hypothesis that high fat (HF) feeding results in endothelial dysfunction in resistance arteries of epididymal white adipose tissue (eWAT) and is mediated by adipose tissue inflammation. When compared with normal chow (NC)-fed mice ( n = 17), HF-fed male B6D2F1 mice were glucose intolerant and insulin resistant as assessed by glucose tolerance test (area under the curve; HF, 18,174 \u00b1 1,889 vs. NC, 15,814 \u00b1 666 mg\u00b7dl\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    ; P &lt; 0.05) and the homeostatic model assessment (HF, 64.1 \u00b1 4.3 vs. NC, 85.7 \u00b1 6.4; P = 0.05). HF diet-induced metabolic dysfunction was concomitant with a proinflammatory eWAT phenotype characterized by greater macrophage infiltration (HF, 3.9 \u00b1 0.8 vs. NC, 0.8 \u00b1 0.4%; P = 0.01) and TNF-\u03b1 (HF, 22.6 \u00b1 4.3 vs. NC, 11.4 \u00b1 2.5 pg\/dl; P &lt; 0.05) and was associated with resistance artery dysfunction, evidenced by impaired endothelium-dependent dilation (EDD) (maximal dilation; HF, 49.2 \u00b1 10.7 vs. NC, 92.4 \u00b1 1.4%; P &lt; 0.01). Inhibition of nitric oxide (NO) synthase by N\n                    <jats:sup>\u03c9<\/jats:sup>\n                    -nitro-l-arginine methyl ester (l-NAME) reduced dilation in NC (28.9 \u00b1 6.3%; P &lt; 0.01)- and tended to reduce dilation in HF (29.8 \u00b1 9.9%; P = 0.07)-fed mice, eliminating the differences in eWAT artery EDD between NC- and HF-fed mice, indicative of reduced NO bioavailability in eWAT resistance arteries after HF feeding. In vitro treatment of excised eWAT arteries with recombinant TNF-\u03b1 (rTNF) impaired EDD ( P &lt; 0.01) in NC (59.7 \u00b1 10.9%)- but not HF (59.0 \u00b1 9.3%)-fed mice. l-NAME reduced EDD in rTNF-treated arteries from both NC (21.9 \u00b1 6.4%)- and HF (29.1 \u00b1 9.2%)-fed mice (both P &lt; 0.01). In vitro treatment of arteries with a neutralizing antibody against TNF-\u03b1 (abTNF) improved EDD in HF (88.2 \u00b1 4.6%; P = 0.05)-fed mice but was without effect on maximal dilation in NC (89.0 \u00b1 5.1%)-fed mice. l-NAME reduced EDD in abTNF-treated arteries from both NC (25.4 \u00b1 7.5%)- and HF (27.1 \u00b1 16.8%)-fed mice (both P &lt; 0.01). These results demonstrate that inflammation in the visceral adipose tissue resulting from diet-induced obesity impairs endothelial function and NO bioavailability in the associated resistance arteries. This dysfunction may have important implications for adipose tissue blood flow and appropriate tissue function.\n                  <\/jats:p>","DOI":"10.1152\/ajpheart.00271.2012","type":"journal-article","created":{"date-parts":[[2012,7,21]],"date-time":"2012-07-21T09:38:05Z","timestamp":1342863485000},"page":"H672-H679","source":"Crossref","is-referenced-by-count":50,"title":["TNF-\u03b1 impairs endothelial function in adipose tissue resistance arteries of mice with diet-induced obesity"],"prefix":"10.1152","volume":"303","author":[{"given":"Anthony J.","family":"Donato","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah;"},{"name":"Geriatrics Research Education and Clinical Center, Veteran's Affairs Medical Center-Salt Lake City, Salt Lake City, Utah;"},{"name":"Department of Physiology, University of Utah, Salt Lake City, Utah;"},{"name":"Department of Exercise and Sports Science, University of Utah, Salt Lake City, Utah"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grant D.","family":"Henson","sequence":"additional","affiliation":[{"name":"Department of Exercise and Sports Science, University of Utah, Salt Lake City, Utah"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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Utah;"},{"name":"Department of Physiology, University of Utah, Salt Lake City, Utah;"},{"name":"Department of Exercise and Sports Science, University of Utah, Salt Lake City, 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