06. The Influence of MED12 Knockdown on Adipogenesis

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The ubiquity of obesity has increased exponentially, and the health burden of obesity-related diseases including type 2 diabetes, metabolic disorders, heart diseases, and some types of cancers is growing. Obesity is characterized by the excess accumulation of fat and adipose tissue and driven by adipogenesis, which is the process in which stem cells differentiate into adipocytes. We utilize human adipose derived stem cells (hASCs) isolated from adult fat tissue to study adipogenesis (the formation of fat tissue). This physiological potential, combined with non-invasive collection methods, make hASCs favorable in the search for new clinical stem cell treatments and for the study of cellular processes and differentiation. We are interested in understanding the function of MED12 in adipogenesis and determining its role in initiating cell type specific gene expression in hopes that this research can be used in treatments for obesity and related metabolic disorders. MED12 is a subunit of the Mediator complex kinase module that is critical in regulating cell-type specific gene expression. We have determined a decrease in MED12 leads to a decrease in adipogenesis as shown by the decrease in staining of lipid vesicles and the decrease in expression of adipogenic factors, CEPBɑ2, SREBP1c, and PPARɣ. This supports that MED12 does indeed play an important role in adipogenesis. We will continue to examine at what point during adipogenesis MED12 is most critical so that MED12 may be used as a therapeutic target to control adipogenesis and treat obesity in the future.