Session: SUN 389-408-Signaling Originating from Membrane Receptors
Poster Board SUN-400
Methods: Mice, HepG2 and humans were challenged with glucagon and follistatin mRNA or protein measured. Primary rat beta-cells were used to explore the impact of 24 h exposure to follistatin (10 and 50 ng/mL) on apoptosis (TUNEL assay) and proliferation (BrdU incorporation). Human islets were exposed to 50 ng/mL of follistatin for different timing up to 24h in order to explore glucagon secretion. Data are mean +/- SE.
Results: Mice injected with glucagon showed a 12.6-fold (p< 0.05) increase in liver follistatin mRNA 1 hour after administration compared to untreated mice. Glucagon increased HepG2 cells follistatin secretion to the media 2-fold compared to control (p<0.05). In humans (n=3) plasma follistatin increased 2 fold 4 hour after (p<0.05) a bolus of glucagon IV. Rat β-cells (n=4) treated with follistatin for 24h showed a decrease in apoptosis when compared to untreated cells (0.17 +/- 0.06 % and 0.42 +/- 0.04 % TUNEL positive cells for 10 and 50 ng/mL follistatin respectively vs. 0.87+/-0.8% for control). Proliferation was increased when compared to untreated cells (7.73+/-0.37 % and 6.27+/- 0.3 % BrdU positive cells for 10 and 50 ng/mL follistatin respectively vs. 4.0+/-0.17 % for control). In human islets treated with 50 ng/mL follistatin glucagon release (n=2) at 16.7 mM glucose was decreased 4-fold after 1 and 2 h follistatin treatment but unchanged after 24h, There was no effect of follistatin on stimulated glucagon secretion (2.8 mM glucose) at any time of treatment.
Conclusion: Our study indicates that glucagon induces hepatic follistatin expression and release. Furthermore that follistatin modulate the pancreatic glucagon response to hypoglycemia. Taken together these data suggest a novel liver pancreas crosstalk consisting of glucagon and follistatin.
Nothing to Disclose: PP, CB, BKP, PH, KB
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