Abstract
In mice heterozygous for the cyclooxygenase-2 gene (COX-2 ±) the body weight was enhanced by 33% as compared to homozygous COX-2 − /− mice. The weights of the gonadal fat pads in COX-2 ± mice were enhanced by 3.5 to 4.7 fold as compared to COX-2 − /− mice and by 1.5 to 3.5 fold as compared to wild-type controls +/+. Serum leptin levels and leptin release by cultured adipose tissue of COX-2 ± mice were both elevated as compared to either control or COX-2 − /− animals. The basal release of PGE 2 or 6 keto PGF 1α per fat pad over a 24 h incubation of adipose tissue was reduced by 80% and 95% respectively in tissue from COX-2 − /− mice. NS-398, a specific COX-2 inhibitor, inhibited leptin release by 27% in adipose tissue from control mice, 31% in tissue from COX-1 − /− mice and by 23% in tissue from COX-2 ± mice while having no effect on leptin release by adipose tissue from COX-2 − /− mice. These data indicate that heterozygous COX-2 mice develop obesity which is not secondary to a defect in leptin release by adipose tissue.
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