Cold-Induced Browning of Inguinal White Adipose Tissue Is Independent of Adipose Tissue Cyclooxygenase-2

Previous studies using genetic mouse models have implicated COX-2 in the browning of white adipose tissues (WATs) in mice during cold exposure. However, COX-2 is important during development, and conventional knockouts (KOs) exhibit many defects, conditioned by genetic background. Similarly, the physiological relevance of transgenic overexpression of COX-2 is questionable. In the present study, we utilized mice in which COX-2 was deleted postnatally, bypassing the consequences of enzyme deficiency during development. Despite activation of thermogenesis and browning of inguinal WAT, cold exposure failed to increase COX-2 expression in the adipose tissues of mice with different genetic backgrounds, and the body temperature response to cold was unaltered in postnatal global COX-2 KOs. Selective disruption of COX-2 in adipose tissues also failed detectably to impact systemic prostaglandin biosynthesis. Browning of inguinal WATs induced by exposure to cold is independent of adipose tissue COX-2. [Display omitted] •COX-2 is undetectable in inguinal adipose tissue by spectrometry and immunoblotting•Cold exposure does not upregulate COX-2 expression in inguinal white adipose tissue•COX-2 is not required for cold-induced browning of inguinal white adipose tissue COX-2 is of importance during development. Browning of inguinal white adipose tissue is involved in metabolic health and reduced susceptibility to obesity. This study tested the involvement of COX-2 in browning of inguinal white adipose tissue and found no role for COX-2.