The acute effects of growth hormone in adipose tissue is associated with suppression of antilipolytic signals

Figure 1. Panel (a) two representative Western blots of phosphorylated STAT5 30 and 120 minutes after intravenous bolus of GH and saline using anti‐STAT5 antibody from Cell Signaling Technology (Cat. No.: #4322). Lower panel: mean ± SE levels of serum GH (a) and serum FFA (b) after exposure to GH (filled circles) and saline (open circles). (p = .003)

Figure 2. Phosphorylation of STAT5 relative to total STAT5 in subcutaneous adipose tissue (a) and serum FFA levels (b) in wild‐type mice (control) and GH receptor knock‐out mice (FaGHRKO) 120 min after intraperitoneal administration of saline or GH. Representative western blots are shown under using anti‐STAT5 antibody from Cell Signaling Technology (Cat. No.: #4322) and anti‐STAT5 antibody from AbCam (# ab194898 ) (a). STAT5 phosphorylation was only detected after GH administration in control mice

Figure 3. (a): Microarray data for genes involved in GH signaling and lipolysis. Differentially expressed genes 120 minutes after stimulation with GH compared to the GH unstimulated state. Note: the presented p values are unadjusted; for further information see results (b): Lower panel: Comparative mRNA determinations of selected target genes with the microarray (open bars) and qRT‐PCR (filled bars). Data are presented as mean ± SE of fold change in mRNA expression of GH exposed samples relative to GH unexposed samples

Figure 4. qPCR analysis of PTEN, RASD1, CISH, PDE3B, and G0S2 mRNA abundance isolated from 3T3‐L1 adipocytes treated with bGH (GH) for 2 hr. Data are shown as mean ± SE of three independent experiments

Figure 5. qPCR analysis of CISH, PDE3B, PTEN, G0S2, and RASD1 mRNA abundance isolated from 3T3‐L1 adipocytes with no treatment (C), treated with 500 µg/l bGH (GH) and/or 100 nmol/l insulin for 2 hr. Data are shown as mean ± SE of three independent experiments. *p; .05, **p; .01, ***p; .001

Figure 6. Schematic model and interpretation of the data regarding the interaction between GH and insulin actions on lipolytic regulators in adipose tissue. GH upregulates PTEN mRNA, which suppresses insulin signaling and thereby insulin‐mediated anti‐lipolysis. GH downregulates mRNA expression of G0S2 and RASD1 both of which suppress lipolysis in an insulin‐dependent manner. Put together, GH predominantly suppresses anti‐lipolytic signal