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Effect of magnesium supplementation and depletion on the onset and course of acute experimental pancreatitis
  1. Verena Schick1,
  2. Jonas A Scheiber2,
  3. Frank C Mooren1,3,
  4. Stefan Turi1,2,
  5. Güralp O Ceyhan1,4,
  6. Jürgen Schnekenburger1,
  7. Matthias Sendler2,
  8. Theresa Schwaiger2,
  9. Armin Omercevic2,
  10. Cindy van den Brandt2,
  11. Gabriele Fluhr2,
  12. Wolfram Domschke1,
  13. Burkhard Krüger5,
  14. Julia Mayerle1,2,
  15. Markus M Lerch1,2
  1. 1Department of Medicine B, Westfälische Wilhelms-Universität, Münster, Germany
  2. 2Department of Medicine A, Universitätsmedizin Greifswald, Greifswald, Germany
  3. 3Department of Sports Medicine, Justus-Liebig-Universität, Giessen, Germany
  4. 4Department of Surgery, Klinikum Rechts der Isar, Technische Universität, München, Germany
  5. 5Division of Medical Biology, Universität Rostock, Rostock, Germany
  1. Correspondence to Markus M Lerch, Department of Medicine A, Universitätsmedizin, Ernst-Moritz-Arndt-Universität Greifswald, Ferdinand-Sauerbruch-Strasse, D-17475 Greifswald, Germany; lerch{at}


Background and objective High calcium concentrations are an established risk factor for pancreatitis. We have investigated whether increasing magnesium concentrations affect pathological calcium signals and premature protease activation in pancreatic acini, and whether dietary or intraperitoneal magnesium administration affects the onset and course of experimental pancreatitis.

Methods Pancreatic acini were incubated with up to 10 mM magnesium; [Ca2+]i (fura-2AM) and intracellular protease activation (fluorogenic substrates) were determined over 60 min. Wistar rats received chow either supplemented or depleted for magnesium (<300 ppm to 30 000 ppm) over two weeks before pancreatitis induction (intravenous caerulein 10 µg/kg/h/4 h); controls received 1 µg/kg/h caerulein or saline. C57BL6/J mice received four intraperitoneal doses of magnesium (NaCl, Mg2+ 55 192 or 384 mg/kg bodyweight) over 72 h, then pancreatitis was induced by up to eight hourly supramaximal caerulein applications. Pancreatic enzyme activities, protease activation, morphological changes and the immune response were investigated.

Results Increasing extracellular Mg2+ concentration significantly reduced [Ca2+]i peaks and frequency of [Ca2+]i oscillations as well as intracellular trypsin and elastase activity. Magnesium administration reduced pancreatic enzyme activities, oedema, tissue necrosis and inflammation and somewhat increased Foxp3-positiv T-cells during experimental pancreatitis. Protease activation was found in animals fed magnesium-deficient chow—even with low caerulein concentrations that normally cause no damage.

Conclusions Magnesium supplementation significantly reduces premature protease activation and the severity of pancreatitis, and antagonises pathological [Ca2+]i signals. Nutritional magnesium deficiency increases the susceptibility of the pancreas towards pathological stimuli. These data have prompted two clinical trials on the use of magnesium in patients at risk for pancreatitis.


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