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- W2018656739 abstract "Endothelin-1 (ET-1) is known to stimulate glycogenolysis in perfused rat livers and isolated rat hepatocytes. To determine the potential action of endothelin's precursor, big endothelin-1 (big ET-1), isolated rat livers were perfused with big ET-1 in a non-recirculating system. Thereby, big ET-1 (10 nM) induced a maximally threefold increase ( P<0.01 vs. basal values) in hepatic glucose production at 60 min, which was almost completely abolished by concomitant infusion of 50 μM phosphoramidon, a sensitive inhibitor of the enzymatic cleavage of big ET-1 to ET-1. The corresponding incremental release of glucose by big ET-1 was 20.9-fold higher in the absence of phosphoramidon than in its presence ( P<0.01 ). In contrast, phosphoramidon did not inhibit hepatic glucose production induced by ET-1 (1 nM), glucagon (1 nM), and phenylephrine (5 μM). Glycogenolytic responses to 1 nM ET-1 ( P<0.01 ), but not to 1 nM glucagon (n.s.) were blocked by indomethacin (100 μM), indicating that prostaglandin release by non-parenchymal cells is at least in part involved in the hepatic ET-1 action. In conclusion, big ET-1 induces hepatic glucose release, which is suggested to depend on intrahepatic conversion of big ET-1 to ET-1 by a phosphoramidon-sensitive pathway." @default.
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- W2018656739 date "1994-05-01" @default.
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- W2018656739 title "Evidence for phosphoramidon-sensitive cleavage of big endothelin-1 involved in endothelin-stimulated hepatic glucose production" @default.
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- W2018656739 doi "https://doi.org/10.1016/0167-0115(94)90066-3" @default.
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