Isolation of mature adipocytes from in vitro differentiated human adipose stem cells

Obesity and associated metabolic outcomes define the metabolic syndrome. Interestingly, an under-appreciated fact is that body fat distribution, rather than total body fat amount, is a key determinant of metabolic disease. Indeed, in contrast to upper-body obesity, lower-body fat accumulation inversely correlates with metabolic risks. Understanding processes regulating upper- vs. lower-body fat expansion is paramount to predict (and prevent) these risks. We combine functional, proteomics, transcriptomics and epigenomics analyses to identify chromatin-associated mechanisms of adipose depot-specific fat expansion. Here, we analyze by RNA-seq the transcriptome of adipocytes differentiated in vitro from human gluteal (lower-body) and abdominal subcutaneous (upper-body) depots-derived adipose stem cells. We aim to identify adipose depot-specific and temporal differences in the up- or down-regulation of gene expression, and relate these differences to changes in chromatin states.