BMAL2 controls adipose tissue inflammation and metabolic adaptation during obesity
We profile the transcripts of adipose progenitors defined as CD45-CD31-PDGFRb+ isolated from eWAT of wild-type and Bmal2-/- C57BL/6J mice fed with normal diet or high-fat diet for 12 weeks. We show that Bmal2 invalidation strongly impacts the transcriptome profile in adipose progenitors and, when associated with obesogenic diet, enhances its deleterious effects. Loss of Bmal2 alters metabolic and maintenance pathways in adipose progenitors and strongly enhances their inflammatory function during diet-induced obesity. Overall design: Bulk RNA-seq profiling of CD45-CD31-PDGFRb+ FACS sorted cells from eWAT of WT and Bmal2-/- (KO) C57BL/6J male mice fed with normal diet (ND) or 12 weeks high-fat diet (HFD).