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. 2017 May 17;292(28):11815–11828. doi: 10.1074/jbc.M117.777748

Figure 3.

Figure 3.

Lipolysis is activated in hepatocytes by isoproterenol. A, confocal images of ORO-stained LDs and the corresponding graph show a significant ∼40% reduction in LD area/cell following 24 h of treatment with isoproterenol (Iso, 50 μm). B, in contrast, isoproterenol had no effect on LD content in the presence of the PKA inhibitor H89 (10 μm). C and D, in addition, inhibition of lipolysis by the ATGL inhibitor atglistatin (C, 10 μm) or the HSL inhibitor CAY10499 (D, 10 μm) also inhibited isoproterenol-mediated LD loss. E and F, Western blot analyses revealed β-AR/cAMP-stimulated HSL phosphorylation (Ser-660) in primary rat hepatocytes (E) and ATGL phosphorylation (Ser-404) in Hep3B cells (F), both of which were inhibited by H89. Dashed circles denote nucleus positions in confocal images. Statistical analysis of fold change was done using a two-tailed paired t test. **, p < 0.01. CT, control.