{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T14:45:54Z","timestamp":1791557154823,"version":"4.3.4"},"reference-count":40,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,9,6]],"date-time":"2012-09-06T00:00:00Z","timestamp":1346889600000},"content-version":"vor","delay-in-days":1193,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Obesity"],"published-print":{"date-parts":[[2009,6]]},"abstract":"<jats:p>The aim was to examine the role of cyclooxygenase (COX)\u20102\u2010mediated inflammation in the development of obese linked insulin resistance and fatty liver. The rats were fed separately regular diet (CONT), high\u2010fat diet (HFD) <jats:italic>ad libitum<\/jats:italic>, or energy restrictedly for 12 weeks. Rats fed HFD <jats:italic>ad libitum<\/jats:italic> were further divided into three subgroups co\u2010treated with vehicle (HFa), or a selective COX\u20102 inhibitor celecoxib (HFa\u2010Cel) or mesulid (HFa\u2010Mes). Euglycemic hyperinsulinemic clamp (EHC) experiment was performed at the end of study. Another set of rats with similar grouping was further divided into those with a 4, 8, or 12\u2010week intervention period for hepatic sampling. Body weight was increased significantly and similarly in HFa, HFa\u2010Cel, and HFa\u2010Mes. Time\u2010dependent increases in plasma insulin, glucose, 8\u2010isoprostanes, leptin levels, homeostasis model assessment of insulin resistance (HOMA\u2010IR) and hepatic triglyceride contents shown in HFa were significantly reversed in HFa\u2010Cel and HFa\u2010Mes. During EHC period, the reduction in stimulation of whole body glucose uptake, suppression of hepatic glucose production and metabolic clearance rate of insulin shown in HFa were significantly reversed in HFa\u2010Cel and HFa\u2010Mes. The enhanced COX\u20102 and tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) but attenuated PPAR\u2010\u03b3 and C\/EBP\u2010\u03b1 mRNA expressions in epididymal fat shown in HFa were significantly reversed in HFa\u2010Cel and HFa\u2010Mes. The increases in average cell size of adipocytes and CD68 positive cells shown in HFa were also significantly reversed in HFa\u2010Cel and HFa\u2010Mes. Our findings suggest that COX\u20102 activation in fat inflammation is important in the development of insulin resistance and fatty liver in high fat induced obese rats.<\/jats:p>","DOI":"10.1038\/oby.2008.674","type":"journal-article","created":{"date-parts":[[2009,2,26]],"date-time":"2009-02-26T15:10:22Z","timestamp":1235661022000},"page":"1150-1157","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":148,"title":["COX\u20102\u2010mediated Inflammation in Fat Is Crucial for Obesity\u2010linked Insulin Resistance and Fatty 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