The Experts below are selected from a list of 186 Experts worldwide ranked by ideXlab platform
R Rude - One of the best experts on this subject based on the ideXlab platform.
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Magnesium Deficiency produces insulin resistance and increased thromboxane synthesis
Hypertension, 1993Co-Authors: J L Nadler, R Natarajan, I Antonipillai, Thomas A Buchanan, Richard N Bergman, R RudeAbstract: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 magnes...
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Magnesium Deficiency produces insulin resistance and increased thromboxane synthesis.
Hypertension (Dallas Tex. : 1979), 1993Co-Authors: J L Nadler, T Buchanan, R Natarajan, I Antonipillai, R Bergman, R RudeAbstract: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.
Toru Nakamura - One of the best experts on this subject based on the ideXlab platform.
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Relation between severity of Magnesium Deficiency and frequency of anginal attacks in men with variant angina
Journal of the American College of Cardiology, 1996Co-Authors: Kazuo Satake, Jong-dae Lee, Hiromasa Shimizu, Takanori Ueda, Toru NakamuraAbstract:AbstractObjectives. We evaluated whether the severity of Magnesium Deficiency was correlated with the frequency of attacks of variant angina.Background. Magnesium Deficiency may be associated with ...
J L Nadler - One of the best experts on this subject based on the ideXlab platform.
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Magnesium Deficiency Is Associated With Insulin Resistance in Obese Children
Diabetes care, 2005Co-Authors: Milagros G. Huerta, James N. Roemmich, Marit L. Kington, Viktor E. Bovbjerg, Arthur Weltman, Viola F. Holmes, James T. Patrie, Alan D. Rogol, J L NadlerAbstract:OBJECTIVE —Magnesium Deficiency has been associated with insulin resistance (IR) and increased risk for type 2 diabetes in adults. This study was designed to determine whether obese children exhibit serum or dietary Magnesium Deficiency and its potential association with IR. RESEARCH DESIGN AND METHODS —We studied 24 obese nondiabetic children (BMI ≥85th percentile) and 24 sex- and puberty-matched lean control subjects (BMI RESULTS —Serum Magnesium was significantly lower in obese children (0.748 ± 0.015 mmol/l, means ± SE) compared with lean children (0.801 ± 0.012 mmol/l) ( P = 0.009). Serum Magnesium was inversely correlated with fasting insulin ( r s = −0.36 [95% CI −0.59 to −0.08]; P = 0.011) and positively correlated with quantitative insulin sensitivity check index ( QUICKI) (0.35 [0.06–0.58]; P = 0.015). Dietary Magnesium intake was significantly lower in obese children (obese: 0.12 ± 0.004 vs. lean: 0.14 ± 0.004 mg/kcal; P = 0.003). Dietary Magnesium intake was inversely associated with fasting insulin (−0.43 [−0.64 to −0.16]; P = 0.002) and directly correlated with QUICKI (0.43 [0.16–0.64]; P = 0.002). CONCLUSIONS —The association between Magnesium Deficiency and IR is present during childhood. Serum Magnesium Deficiency in obese children may be secondary to decreased dietary Magnesium intake. Magnesium supplementation or increased intake of Magnesium-rich foods may be an important tool in the prevention of type 2 diabetes in obese children.
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Magnesium Deficiency produces insulin resistance and increased thromboxane synthesis
Hypertension, 1993Co-Authors: J L Nadler, R Natarajan, I Antonipillai, Thomas A Buchanan, Richard N Bergman, R RudeAbstract: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 magnes...
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Magnesium Deficiency produces insulin resistance and increased thromboxane synthesis.
Hypertension (Dallas Tex. : 1979), 1993Co-Authors: J L Nadler, T Buchanan, R Natarajan, I Antonipillai, R Bergman, R RudeAbstract: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.
William B. Weglicki - One of the best experts on this subject based on the ideXlab platform.
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Magnesium Deficiency prolongs myocardial stunning in an open-chest swine model.
International journal of cardiology, 1994Co-Authors: William R. Herzog, Dan Atar, I. Tong Mak, David Alyono, Christopher Maccord, William B. WeglickiAbstract:Abstract The effect of Magnesium Deficiency on postischemic myocardial dysfunction (myocardial stunning) in an open-chest swine model was studied. Twelve swine were assigned either to low Magnesium diet or control diet. Myocardial stunning was assessed by measuring regional wall thickening by epicardial Doppler before and after brief occlusion (8 min) of the left anterior descending coronary artery. Serum Magnesium levels decreased significantly in the experimental group only. Glutathione levels were 42.6% lower in the Magnesium deficient swine than in controls. Stunning time was significantly prolonged from 32.8 ± 3.1 min in the control group to 43.8 ± 4.6 min in the hypomagnesemic swine. In conclusion, Magnesium Deficiency is associated with prolonged recovery from myocardial stunning.
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Magnesium Deficiency elevates circulating levels of inflammatory cytokines and endothelin
Molecular and Cellular Biochemistry, 1992Co-Authors: William B. Weglicki, Terry M Phillips, Anthony M Freedman, Marie M Cassidy, B F DickensAbstract:We have developed two rodent models of diet-induced Magnesium-Deficiency in which histologically defined cardiac lesions can be induced within two to three weeks. During the development of these lesions, the Magnesium-deficient animals exhibit circulating cytokine levels which are indicative of a generalized inflammatory state. Dramatic elevations of the macrophage-derived cytokines, IL-1, IL-6, and TNF-alpha together with significantly elevated levels of the endothelial cell-derived cytokine, endothelin, were detected in the plasma of these animals. We believe that the pathophysiological effects caused by the action of these cytokines may play a role in the promotion of cardiovascular pathology associated with Magnesium Deficiency.
Puneet Agarwal - One of the best experts on this subject based on the ideXlab platform.
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Pathogenetic role of Magnesium Deficiency in ophthalmic diseases
BioMetals, 2014Co-Authors: Renu Agarwal, Lgor Iezhitsa, Puneet AgarwalAbstract:Magnesium is one of the most important regulatory cation involved in several biological processes. It is important for maintaining the structural and functional integrity of several vital ocular tissues such as cornea, lens and retina. The Magnesium content of lens, especially in its peripheral part, is higher than that in aqueous and vitreous humor. Magnesium has also been shown to play critically important role in retinal functions. Magnesium plays significant role as a cofactor for more than 350 enzymes in the body and regulates neuroexcitability and several ion channels. Membrane associated ATPase functions that are crucial in regulating the intracellular ionic environment, are Magnesium-dependent. Moreover, the enzymes involved in ATP production and hydrolysis are also Magnesium-dependent. Magnesium Deficiency by interfering with ATPase functions causes increased intracellular calcium and sodium and decreases intracellular potassium concentration. Such ionic imbalances in turn alter the other cellular enzymatic reactions and form the basis of the association of Magnesium Deficiency with ophthalmic diseases such as cataract. In presence of Magnesium Deficiency, an imbalance between mediators of vasoconstriction and vasorelaxation may underlie the vasospasm, which is one of the pathogenic factors in primary open angle glaucoma. Furthermore, Magnesium Deficiency is also a contributing factor in increased oxidative stress and inducible NOS stimulation that can further contribute in the initiation and progression of ocular pathologies such as cataract, glaucoma and diabetic retinopathy. In this paper we review the association of disturbances of Magnesium homeostasis with several ophthalmic diseases.
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Magnesium Deficiency does it have a role to play in cataractogenesis
Experimental Eye Research, 2012Co-Authors: Renu Agarwal, Puneet Agarwal, Igor Nikolayevich Iezhitsa, Alexander SpasovAbstract:Abstract Magnesium is one of the most important regulatory cation involved in several biological processes. It is important for maintaining the structural and functional integrity of vital ocular tissues such as lens. Presence of high Magnesium content especially in the peripheral part of lens as compared to aqueous and vitreous humor has been observed. Magnesium plays significant role as a cofactor for more than 350 enzymes in the body especially those utilizing ATP. Membrane associated ATPase functions that are crucial in regulating the intracellular ionic environment, are Magnesium-dependent. Moreover, the enzymes involved in ATP production and hydrolysis are also Magnesium-dependent. Magnesium Deficiency by interfering with ATPase functions causes increased intracellular calcium and sodium and decreases intracellular potassium concentration. Furthermore, Magnesium Deficiency is associated with increased oxidative stress secondary to increased expression of inducible nitric oxide synthase and increased production of nitric oxide. Thus the alterations in lenticular redox status and ionic imbalances form the basis of the association of Magnesium Deficiency with cataract. In this paper we review the mechanisms involved in Magnesium homeostasis and the role of Magnesium Deficiency in the pathogenesis of cataract.
