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. 2010 Jul 26;5(7):e11749. doi: 10.1371/journal.pone.0011749

Figure 3. Confirmation of UAG regulated genes in white adipose tissue.

Figure 3

Quantitative PCR measurement of gene expression in an independent experiment confirms regulation by UAG of genes involved in lipid/cholesterol metabolism, as well as adipocyte differentiation and insulin-sensitivity in white adipose tissue (WAT). A: Key regulators of fatty acid synthesis, both short and long-chain, were suppressed by UAG treatment. B: Hormone sensitive lipase (Lipe) and liporotein lipase (Lipd) gene expression is increased. C: Regulators of cholesterol synthesis, Insig1 and Hmgcs1 are suppressed by UAG, whereas Srebp1c is induced. D: Expression of Pparg and its coactivator Ppargc1a, mRNAs that encode key regulators of lipid synthesis were suppressed by UAG. Pparg is also a key regulator of adipocyte differentiation. E: Key transcriptional regulators of adipocyte differentiation, Cebpa and Cebpd are up and down-regulated, respectively, by UAG in fat, suggesting suppressive effects on the early stages of differentiation. F: Regulation of Serpine1, Lcn2 and Ucp2 by UAG indicates improvement of insulin sensitivity in WAT. G: Components of the Notch signalling (Notch1/4, Jagged1) and the fibrinolytic (Mmp9) pathways (inhibitory and permissive for adipocyte differentiation, respectively) are regulated by UAG.