Components of the signaling pathway for glucagon (GLU) and glucagon-like peptide-1 (GLP-1) were investigated in hepatocytes and membranes of two teleost fishes, the American eel (Anguilla rostrata) and the black bullhead (Ictalurus melas). Glucagon stimulated glucose release from isolated hepatocytes while increasing in a time- and dose-dependent fashion cAMP and inositol 1,4,5-trisphosphate (IP3) concentrations. Phospholipase C (PLC), but not adenylyl cyclase (ACase), activities were statistically increased in hepatic membranes. GLP-1 also stimulated glucose release and a small but statistically significant increase in cAMP but not IP3 concentrations in hepatocytes. The glucagon-family peptide also statistically stimulated PLC, but not ACase activities. Responses to epinephrine (EPI) were generally similar with respect to glucose release and enzyme activation, but changes to cAMP were much greater than that of either GLU or GLP-1. These results support those in mammalian hepatocytes, which suggest that GLU may act through both the cAMP and the IP3 signaling pathways. However, they do not provide further insight into the mechanism by which GLP-1 may exert its metabolic effects on the fish liver. Although small changes in cAMP were noted, the possibility of an IP3 effect cannot be discounted.
Glucagon and glucagon-like peptide signaling pathways in the liver of two fish species, the American eel and the black bullhead
CAPUZZO, Antonio;
1997
Abstract
Components of the signaling pathway for glucagon (GLU) and glucagon-like peptide-1 (GLP-1) were investigated in hepatocytes and membranes of two teleost fishes, the American eel (Anguilla rostrata) and the black bullhead (Ictalurus melas). Glucagon stimulated glucose release from isolated hepatocytes while increasing in a time- and dose-dependent fashion cAMP and inositol 1,4,5-trisphosphate (IP3) concentrations. Phospholipase C (PLC), but not adenylyl cyclase (ACase), activities were statistically increased in hepatic membranes. GLP-1 also stimulated glucose release and a small but statistically significant increase in cAMP but not IP3 concentrations in hepatocytes. The glucagon-family peptide also statistically stimulated PLC, but not ACase activities. Responses to epinephrine (EPI) were generally similar with respect to glucose release and enzyme activation, but changes to cAMP were much greater than that of either GLU or GLP-1. These results support those in mammalian hepatocytes, which suggest that GLU may act through both the cAMP and the IP3 signaling pathways. However, they do not provide further insight into the mechanism by which GLP-1 may exert its metabolic effects on the fish liver. Although small changes in cAMP were noted, the possibility of an IP3 effect cannot be discounted.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
