Feedback‐inhibition of glucagon‐stimulated glycogenolysis in hepatocyte/kupffer cell cocultures by glucagon‐elicited prostaglandin production in kupffer cells
Ursula Hespeling, Kurt Jungermann, Gerhard P. Püschel – 1 November 1995 – Prostaglandins, released from Kupffer cells, have been shown to mediate the increase in hepatic glycogenolysis by various stimuli such as zymosan, endotoxin, immune complexes, and anaphylotoxin C3a involving prostaglandin (PG) receptors coupled to phospholipase C via a G0 protein. PGs also decreased glucagon‐stimulated glycogenolysis in hepatocytes by a different signal chain involving PGE2 receptors coupled to adenylate cyclase via a Gi protein (EP3 receptors).