Obesity is caused by energy intake that chronically exceeds energy expenditure. Emerging evidence suggests that white adipose tissues can be reprogrammed to express mitochondrial uncoupling protein 1 (UCP1) to promote thermogenesis. This transformation, referred as “browning” of white adipose tissue, can increase energy expenditure and prevent obesity. Mice with a whole body knockout of phosphatidylethanolamine methyltransferase (PEMT) are protected from diet‐induced obesity due to an increase in whole‐body energy expenditure. However, the mechanism that promotes energy expenditure in these mice is unknown. We hypothesized that the absence of PEMT results in the browning of white adipose tissues. In this study, we examined adipose tissues from wild type (WT) and whole‐body PEMT knockout (PEMTKO) mice fed with a 10 week high‐fat diet. Inguinal and epididymal white adipose tissue (iWAT and eWAT) were analyzed for UCP1 expression by quantitative‐PCR, western blotting and immunohistochemistry. We found that mice lacking PEMT exhibited elevated RNA and protein abundance of UCP1 in iWAT and to a lesser extent in eWAT. These findings support our hypothesis that browning of white adipose tissue may contribute to increased energy expenditure in mice lacking PEMT. In future experiments, we will determine whether the absence of PEMT specifically in adipose tissues will promote browning and increased energy expenditure.Support or Funding InformationThis work was supported by NIH grant DK095774 to KF and APS/NHLBI STRIDE fellowship 1 R25 HL115473‐01 to SS.