Glucose modulates Mg2+ fluxes in pancreatic islet cells.
Magnesium, the most abundant intracellular divalent cation, is an essential cofactor for many enzyme systems, but it remains unknown as to whether variations in the cytoplasmic concentration of ionized Mg2+ directly control cellular processes. Experiments with adrenal medullary cells made 'leaky' by exposure to high electric fields provided evidence that Mg2+ could influence hormone release not only by competing with Ca2+ for entry into the cell, but also at intracellular sites controlling exocytosis. A similar conclusion was reached for insulin release in a study using isolated rat islets also subjected to high voltage discharges. There is no experimental evidence, however, that physiological stimuli influence Mg2+ movements in intact secretory cells. We report here that 28Mg2+ fluxes in pancreatic islet cells are markedly modified by glucose, the physiological stimulus of insulin release, but not by its non-insulinotropic analogue, 3-O-methylglucose.
D019325:3-O-Methylglucose; D000818:Animals; D005947:Glucose / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism*; D008757:Methylglucosides / Q000494:pharmacology; D051381:Rats; D013997:Time Factors
D008757:Methylglucosides; D019325:3-O-Methylglucose; D008274:Magnesium; D005947:Glucose