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Effects of tri-Calciphor (trimer of 16, 16-dimethyl-15-dehydroprostaglandin B1) on glucose metabolism in liver cells
Journal article   Peer reviewed

Effects of tri-Calciphor (trimer of 16, 16-dimethyl-15-dehydroprostaglandin B1) on glucose metabolism in liver cells

R Villalobos-Molina and T M Devlin
Biochemical and biophysical research communications, v 201(3), pp 1457-1463
30 Jun 1994
PMID: 8024591

Abstract

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.

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Web of Science research areas
Biochemistry & Molecular Biology
Biophysics
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