The molecular circadian clock is a transcription-translation feedback loop which serves as a timekeeping mechanism in most nucleated mammalian cells. Work from our lab and others has been directed at understanding the contribution of the clock to adipocyte function and response to obesity. In particular, we have focused on the role of REV-ERBalpha (NR1D1), a core clock protein and transcriptional repressor. In a transgenic mouse with adipocyte-targeted Nr1d1 deletion, we see enhanced adiposity with diet-induced obesity, with diminished ectopic lipid deposition, and relative sparing from obesity-related pathology. In my talk, I will discuss our past and present efforts to understand the mechanism underlying this remarkable ‘healthy’ obesity phenotype.