November 12, 2014
Notes: Sang, Gao
Peptides. 2014 Jan;51:4-8. doi: 10.1016/j.peptides.2013.10.019. Epub 2013 Oct 30.
Author Address: Department of Paediatrics, Tongde Hospital Zhejiang Chinese Medical University, 234 Gucui Road, Hangzhou 310012, China.
Department of Paediatrics, The First People’s Hospital of Hangzhou, Nanjing Medical University, 261 Huansha Road, Hangzhou 310006, China.
Department of Traditional Chinese Internal Medicine, Tongde Hospital Zhejiang Chinese Medical University, 234 Gucui Road, Hangzhou 310012, China. Electronic address: email@example.com.
Intensive Care Unit, Tongde Hospital Zhejiang Chinese Medical University, 234 Gucui Road, Hangzhou 310012, China.
Department of Gastroenterology, Tongde Hospital Zhejiang Chinese Medical University, 234 Gucui Road, Hangzhou 310012, China.
Reference Type: Journal Article
Record Number: 4769Author: Schick, V., Scheiber, J. A., Mooren, F. C., Turi, S., Ceyhan, G. O., Schnekenburger, J., Sendler, M., Schwaiger, T., Omercevic, A., Brandt, Cv, Fluhr, G., Domschke, W., Kruger, B., Mayerle, J. and Lerch, M. M.
Title: Effect of magnesium supplementation and depletion on the onset and course of acute experimental pancreatitis
Short Title: Effect of magnesium supplementation and depletion on the onset and course of acute experimental pancreatitis
Alternate Journal: Gut
ISSN: 1468-3288 (Electronic)
Accession Number: 24277728
Keywords: Acute Disease
Pancreatitis/etiology/immunology/metabolism/*prevention & control
Severity of Illness Index
Abstract: 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; [Ca(2+)](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 microg/kg/h/4 h); controls received 1 microg/kg/h caerulein or saline. C57BL6/J mice received four intraperitoneal doses of magnesium (NaCl, Mg(2+) 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 Mg(2+) concentration significantly reduced [Ca(2+)](i) peaks and frequency of [Ca(2+)](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 [Ca(2+)](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.