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10.1161/01.hyp.21.6.1024 http://scihub22266oqcxt.onion/10.1161/01.hyp.21.6.1024 8505087!ä!8505087 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\8505087.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Hypertension 1993 ; 21 (6 Pt 2): 1024-9 Nephropedia Template TP {{tp|p=8505087|t=1993. Magnesium deficiency produces insulin resistance and increased thromboxane synthesis |pdf=|usr=}}{{8505087}} gab.com Text Magnesium deficiency produces insulin resistance and increased thromboxane synthesis JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=8505087 #FOAvip Evidence suggests that magnesium deficiency may play an important role in cardiovascular disease. In this study, we evaluated the effects of a magnesium infusion and dietary-induced isolated magnesium deficiency on the production of thromboxane and on angiotensin II-mediated aldosterone synthesis in normal human subjects. Because insulin resistance may be associated with altered blood pressure, we also measured insulin sensitivity using an intravenous glucose tolerance test with minimal model analysis in six subjects. The magnesium infusion reduced urinary thromboxane concentration and angiotensin II-induced plasma aldosterone levels. The low magnesium diet reduced both serum magnesium and intracellular free magnesium in red blood cells as determined by nuclear magnetic resonance (186 +/- 10 [SEM] to 127 +/- 9 mM, p < 0.01). Urinary thromboxane concentration measured by radioimmunoassay increased after magnesium deficiency. Similarly, angiotensin II-induced plasma aldosterone concentration increased after magnesium deficiency. Analysis showed that all subjects studied had a decrease in insulin sensitivity after magnesium deficiency (3.69 +/- 0.6 to 2.75 +/- 0.5 min-1 per microunit per milliliter x 10(-4), p < 0.03). We conclude that dietary-induced magnesium deficiency 1) increases thromboxane urinary concentration and 2) enhances angiotensin-induced aldosterone synthesis. These effects are associated with a decrease in insulin action, suggesting that magnesium deficiency may be a common factor associated with insulin resistance and vascular disease. Twit Text FOAVip Magnesium deficiency produces insulin resistance and increased thromboxane synthesis ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=8505087 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=8505087 #FOAvip English Wikipedia <ref>{{Cite pmid|8505087}}</ref> Magnesium deficiency produces insulin resistance and increased thromboxane synthesis #MMPMID8505087 Nadler JL; Buchanan T; Natarajan R; Antonipillai I; Bergman R; Rude R Hypertension 1993[Jun]; 21 (6 Pt 2): 1024-9 PMID8505087show ga Evidence suggests that magnesium deficiency may play an important role in cardiovascular disease. In this study, we evaluated the effects of a magnesium infusion and dietary-induced isolated magnesium deficiency on the production of thromboxane and on angiotensin II-mediated aldosterone synthesis in normal human subjects. Because insulin resistance may be associated with altered blood pressure, we also measured insulin sensitivity using an intravenous glucose tolerance test with minimal model analysis in six subjects. The magnesium infusion reduced urinary thromboxane concentration and angiotensin II-induced plasma aldosterone levels. The low magnesium diet reduced both serum magnesium and intracellular free magnesium in red blood cells as determined by nuclear magnetic resonance (186 +/- 10 [SEM] to 127 +/- 9 mM, p < 0.01). Urinary thromboxane concentration measured by radioimmunoassay increased after magnesium deficiency. Similarly, angiotensin II-induced plasma aldosterone concentration increased after magnesium deficiency. Analysis showed that all subjects studied had a decrease in insulin sensitivity after magnesium deficiency (3.69 +/- 0.6 to 2.75 +/- 0.5 min-1 per microunit per milliliter x 10(-4), p < 0.03). We conclude that dietary-induced magnesium deficiency 1) increases thromboxane urinary concentration and 2) enhances angiotensin-induced aldosterone synthesis. These effects are associated with a decrease in insulin action, suggesting that magnesium deficiency may be a common factor associated with insulin resistance and vascular disease. |*Insulin Resistance[MESH] |Aldosterone/blood[MESH] |Angiotensin II/pharmacology[MESH] |Diet[MESH] |Female[MESH] |Glucose Tolerance Test[MESH] |Humans[MESH] |Injections, Intravenous[MESH] |Intracellular Membranes/metabolism[MESH] |Magnesium Deficiency/*metabolism/*physiopathology[MESH] |Magnesium/blood/pharmacology[MESH] |Male[MESH]Magnesium deficiency produces insulin resistance and increased thrombo(epmc).pdf DeepDyve Pubget Overpricing