Effects of tri-Calciphor (trimer of 16, 16-dimethyl-15-dehydroprostaglandin B1) on glucose metabolism in liver cells.
Phosphorylase activity of isolated rat liver cells was increased about 2-fold on addition of tri-Calciphor (trimer of 16, 16-dimethyl-15-dehydroprostaglandin B1), epinephrine or the Ca2+ ionophore A23187, in all cases presumably due to an increase in cytosolic Ca2+. Extracellular Ca2+ was required with A23187, but not with either tri-Calciphor or epinephrine. Tri-Calciphor, however, did not stimulate a sustained release of glucose from hepatocytes as compared to the other Ca2+ mobilizing agents, even at concentrations 10-fold higher than that required to stimulate the phosphorylase activity. Tri-Calciphor did not alter the glucose release by epinephrine. It is concluded that tri-Calciphor can alter cytosolic Ca2+, but that its mechanism of action is more complex than that of a simple Ca2+ ionophore.
Villalobos-Molina
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Department of Biological Chemistry, Hahnemann University School of Medicine, Philadelphia, PA 19102-1192.
Devlin
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TM
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D004789:Enzyme Activation; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D005947:Glucose / Q000378:metabolism*; D007476:Ionophores; D008099:Liver / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism; D006005:Phosphorylases / Q000378:metabolism; D011456:Prostaglandins B / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar
C052137:16,16-dimethyl-15-dehydroprostaglandin B1 trimer; D007476:Ionophores; D008112:Liver Glycogen; D011456:Prostaglandins B; D000001:Calcimycin; D006005:Phosphorylases; D005947:Glucose; D004837:Epinephrine