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Lawrence M Resnick - One of the best experts on this subject based on the ideXlab platform.
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Magnesium Metabolism in hypertension and type 2 diabetes mellitus
American Journal of Therapeutics, 2007Co-Authors: Mario Barbagallo, Ligia J Dominguez, Lawrence M ResnickAbstract:The increasing evidence for the clinical relevance of altered Magnesium Metabolism to states of altered insulin resistance confirms the role of Magnesium deficit as a possible underlying common mechanism of the "insulin resistance" of hypertension and altered glucose tolerance. The pioneer work of Lawrence M. Resnick and his group using the cellular ion-based approach that we are only partially presenting here has consistently contributed to the progress of the field, demonstrating (a) the critical importance of Magnesium Metabolism in regulating insulin sensitivity as well as vascular tone, and blood-pressure homeostasis; (b) that Magnesium deficiency, defined on the basis of intracellular free Magnesium levels, and or serum ionized Magnesium is a common feature of both diabetic and hypertensive states as well as various other cardiovascular and metabolic processes and aging; (c) the ability of environmental factors such as dietary nutrient-sugar and mineral content to alter the set point of steady-state cell ion activity; and (d) that Magnesium supplementation is indicated in conditions associated with Magnesium deficit although well-designed therapeutic trials of Magnesium in essential hypertension and type 2 diabetes mellitus are needed in the near future.
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cellular free Magnesium depletion in brain and muscle of normal and preeclamptic pregnancy a nuclear magnetic resonance spectroscopic study
Hypertension, 2004Co-Authors: Lawrence M Resnick, Mordechai Bardicef, Orit Bardicef, Yoram Sorokin, Mario Barbagallo, Jeffrey L Evelhoch, Ligia J Dominguez, Brian A Mason, David B CottonAbstract:Preeclampsia is a pregnancy disorder of unknown origin, characterized by vasospasm, elevated blood pressure, and increased neuromuscular irritability, features common to syndromes of Magnesium deficiency. Evidence of serum and ionized Magnesium Metabolism disturbances have been observed in women with preeclampsia. This and the therapeutic utility of Magnesium in preeclampsia led us to investigate the extent to which an endogenous tissue Magnesium deficiency might be present in and contribute to its pathophysiology. We used (31)P nuclear magnetic resonance spectroscopy to noninvasively measure in situ intracellular-free Magnesium levels in brain and skeletal muscle of fasting nonpregnant women (n=12), and of third trimester women with uncomplicated pregnancies (n=11) and preeclampsia (n=7). Compared with nonpregnant controls (brain 519+/-59 micromol/L; muscle 604+/-34 micromol/L), brain and skeletal muscle intracellular Magnesium levels were significantly lower in both normal pregnant (brain 342+/-23 micromol/L; muscle 482+/-40 micromol/L; P=0.05 for both tissues) and preeclamptic women (brain 229+/-17 micromol/L; muscle 433+/-46 micromol/L; P=0.05 for both tissues). Brain intracellular Magnesium was further reduced in preeclamptics compared with normal pregnant subjects (P=0.05). For all pregnant subjects, blood pressure was significantly and inversely related to the concomitantly measured intracellular Magnesium level in brain (systolic, r=-0.59, P=0.01; diastolic, r=-0.52, P=0.02) but not in muscle. Cellular Magnesium depletion is characteristic of normal pregnancy and may be one factor contributing to the pathophysiology of preeclampsia. Furthermore, the influence of central nervous system factors on blood pressure may be mediated, at least in part, by ambient intracellular Magnesium levels.
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intracellular and extracellular Magnesium depletion in type 2 non insulin dependent diabetes mellitus
Diabetologia, 1993Co-Authors: Lawrence M Resnick, Burton M Altura, Raj K Gupta, John H Laragh, Michael H AldermanAbstract:To investigate alterations of Magnesium Metabolism in Type 2 (non-insulin-dependent) diabetes mellitus, we utilized a new Magnesium-specific selective ion electrode apparatus to measure serum ionized Magnesium (Mg-io) in fasting subjects with and without Type 2 diabetes, and compared these values to levels of serum total Magnesium, and of intracellular free Magnesium (Mgi) analysed by 31P-NMR spectroscopy. Both Mg-io (0.630±0.008 vs 0.552± 0.008 mmol/l, p<0.001) and Mgi (223.3±8.3 vs 184± 13.7 mmol/l,p<0.001), but not serum total Magnesium, were significantly reduced in Type 2 diabetes compared with nondiabetic control subjects. Furthermore, a close relationship was observed between serum Mg-io and Mgi (r=0.728, p<0.001). We suggest that Magnesium deficiency, both extracellular and intracellular, is a characteristic of chronic stable mild Type 2 diabetes, and as such, may predispose to the excess cardiovascular morbidity of the diabetic state. Furthermore, by more adequately reflecting cellular Magnesium Metabolism than total serum Magnesium levels, Mg-io measurements may provide a more readily available tool than has heretofore been available to analyse Magnesium Metabolism in a variety of diseases.
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cellular calcium and Magnesium Metabolism in the pathophysiology and treatment of hypertension and related metabolic disorders
The American Journal of Medicine, 1992Co-Authors: Lawrence M ResnickAbstract:We have investigated the cellular basis for the clinical and epidemiologic linkage of hypertension, left ventricular hypertrophy (LVH), obesity, and non-insulin-dependent diabetes mellitus (NIDDM) and have studied cytosolic free calcium and free Magnesium levels in these syndromes. Specifically, intracellular free calcium is elevated and free Magnesium is deficient in hypertension, and both are related (directly and inversely, respectively) to the ambient level of blood pressure, to LV mass index (and thus to the degree of cardiac hypertrophy), and to the hyperinsulinemia and insulin resistance of essential hypertension. Dynamically, the ability of dietary salt loading to elevate blood pressure corresponds to its ability to elevate cytosolic free calcium and reciprocally to suppress free Magnesium levels. Conversely, the ability of calcium channel blockade to reverse salt-induced hypertension is related to its ability to prevent these transmembrane ionic effects. Higher steady-state free calcium or lower free Magnesium, or both, are also observed in clinical states linked to hypertension, such as obesity and NIDDM. Oral glucose loading in normal subjects itself elevates free calcium and suppresses free Magnesium levels, as does hyperglycemia in vitro. These data suggest an ionic hypothesis of cardiovascular and metabolic disease, in which a generalized defect in cell ion handling is present in all tissues, resulting in higher steady-state free calcium and lower free Magnesium levels. In pancreatic beta cells, this would produce hyperinsulinemia; in fat and skeletal muscle, cause peripheral insulin resistance; and in renal tissue, increase proximal sodium resorption and increase urinary calcium excretion--all features of essential hypertension. In vascular smooth muscle, high cytosolic free calcium would increase smooth muscle tone and cause vasoconstriction, and in heart muscle, independent of blood pressure, would increase contractility and predispose to LVH. Therefore, what may appear clinically to be the separate syndromes of hypertension, obesity, and NIDDM may pathophysiologically be different manifestations of the same underlying cellular defect, thus explaining their frequent clinical coexistence. Therapeutically, reversal of this excess free calcium accumulation and/or free Magnesium deficit with ion-specific agents, such as calcium channel blocking drugs, may thus ameliorate not only the elevated blood pressure of hypertension but also the concurrent excess morbidity and mortality of the concurrent cardiac, vascular, and metabolic aspects of the hypertensive state.
Ligia J Dominguez - One of the best experts on this subject based on the ideXlab platform.
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Magnesium Metabolism in hypertension and type 2 diabetes mellitus
American Journal of Therapeutics, 2007Co-Authors: Mario Barbagallo, Ligia J Dominguez, Lawrence M ResnickAbstract:The increasing evidence for the clinical relevance of altered Magnesium Metabolism to states of altered insulin resistance confirms the role of Magnesium deficit as a possible underlying common mechanism of the "insulin resistance" of hypertension and altered glucose tolerance. The pioneer work of Lawrence M. Resnick and his group using the cellular ion-based approach that we are only partially presenting here has consistently contributed to the progress of the field, demonstrating (a) the critical importance of Magnesium Metabolism in regulating insulin sensitivity as well as vascular tone, and blood-pressure homeostasis; (b) that Magnesium deficiency, defined on the basis of intracellular free Magnesium levels, and or serum ionized Magnesium is a common feature of both diabetic and hypertensive states as well as various other cardiovascular and metabolic processes and aging; (c) the ability of environmental factors such as dietary nutrient-sugar and mineral content to alter the set point of steady-state cell ion activity; and (d) that Magnesium supplementation is indicated in conditions associated with Magnesium deficit although well-designed therapeutic trials of Magnesium in essential hypertension and type 2 diabetes mellitus are needed in the near future.
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Magnesium Metabolism in type 2 diabetes mellitus metabolic syndrome and insulin resistance
Archives of Biochemistry and Biophysics, 2007Co-Authors: Mario Barbagallo, Ligia J DominguezAbstract:Type 2 diabetes is characterized by cellular and extracellular Mg depletion. Epidemiologic studies showed a high prevalence of hypomagnesaemia and lower intracellular Mg concentrations in diabetic subjects. Insulin and glucose are important regulators of Mg Metabolism. Intracellular Mg plays a key role in regulating insulin action, insulin-mediated-glucose uptake and vascular tone. Reduced intracellular Mg concentrations result in a defective tyrosine-kinase activity, post-receptorial impairment in insulin action, and worsening of insulin resistance in diabetic patients. Mg deficit has been proposed as a possible underlying common mechanism of the "insulin resistance" of different metabolic conditions. Low dietary Mg intake is also related to the development of type 2 diabetes. Benefits of Mg supplementation on metabolic profile in diabetic subjects have been found in most, but not all clinical studies, and larger prospective studies are needed to support the potential role of dietary Mg supplementation as a possible public health strategy in diabetes risk.
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Magnesium Metabolism in insulin resistance metabolic syndrome and type 2 diabetes mellitus
2007Co-Authors: Mario Barbagallo, Ligia J Dominguez, Virna Brucato, Antonio Galioto, A Pineo, A Ferlisi, Ernesto Tranchina, Mario Belvedere, Ernesto Putignano, Giuseppe CostanzaAbstract:Magnesium plays a key role in regulating insulin action, insulin-mediated glucose uptake, and vascular tone. Intracellular Magnesium depletion may result in a defective tyrosine—kinase activity at the insulin receptor level, in a postreceptorial impairment in insulin action, and clinically in a worsening of insulin resistance. Intra- and extracellular alterations of Magnesium Metabolism have been identified in clinical states characterized by insulin resistance, such as metabolic syndrome, hypertension, altered glucose tolerance, type 2 diabetes, and aging. Several studies, from our and other’s groups, have confi rmed the clinical relevance of alterations of Magnesium homeostasis in these conditions and have highlighted the importance of an accurate definition of the Magnesium status. While measurements of total serum Magnesium levels have been proven inadequate for this purpose because important Magnesium depletions are required before total serum level decreases, two technologies, 31P nuclear magnetic resonance (31P-NMR) spectroscopy and Magnesium-specifi c ion-selective electrodes, that, respectively, measure intracellular and extracellular free levels of Magnesium, have a higher sensitivity in detecting Magnesium deficits. A number of evidences have confirmed that Magnesium supplementation is indicated in conditions associated with Magnesium deficit, although well-designed therapeutic trials with oral Magnesium supplements to study the beneficial effects in metabolic syndrome and in type 2 diabetes are needed.
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cellular free Magnesium depletion in brain and muscle of normal and preeclamptic pregnancy a nuclear magnetic resonance spectroscopic study
Hypertension, 2004Co-Authors: Lawrence M Resnick, Mordechai Bardicef, Orit Bardicef, Yoram Sorokin, Mario Barbagallo, Jeffrey L Evelhoch, Ligia J Dominguez, Brian A Mason, David B CottonAbstract:Preeclampsia is a pregnancy disorder of unknown origin, characterized by vasospasm, elevated blood pressure, and increased neuromuscular irritability, features common to syndromes of Magnesium deficiency. Evidence of serum and ionized Magnesium Metabolism disturbances have been observed in women with preeclampsia. This and the therapeutic utility of Magnesium in preeclampsia led us to investigate the extent to which an endogenous tissue Magnesium deficiency might be present in and contribute to its pathophysiology. We used (31)P nuclear magnetic resonance spectroscopy to noninvasively measure in situ intracellular-free Magnesium levels in brain and skeletal muscle of fasting nonpregnant women (n=12), and of third trimester women with uncomplicated pregnancies (n=11) and preeclampsia (n=7). Compared with nonpregnant controls (brain 519+/-59 micromol/L; muscle 604+/-34 micromol/L), brain and skeletal muscle intracellular Magnesium levels were significantly lower in both normal pregnant (brain 342+/-23 micromol/L; muscle 482+/-40 micromol/L; P=0.05 for both tissues) and preeclamptic women (brain 229+/-17 micromol/L; muscle 433+/-46 micromol/L; P=0.05 for both tissues). Brain intracellular Magnesium was further reduced in preeclamptics compared with normal pregnant subjects (P=0.05). For all pregnant subjects, blood pressure was significantly and inversely related to the concomitantly measured intracellular Magnesium level in brain (systolic, r=-0.59, P=0.01; diastolic, r=-0.52, P=0.02) but not in muscle. Cellular Magnesium depletion is characteristic of normal pregnancy and may be one factor contributing to the pathophysiology of preeclampsia. Furthermore, the influence of central nervous system factors on blood pressure may be mediated, at least in part, by ambient intracellular Magnesium levels.
L I G Worthley - One of the best experts on this subject based on the ideXlab platform.
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the essentials of calcium Magnesium and phosphate Metabolism part ii disorders
Critical Care and Resuscitation, 2002Co-Authors: S B Baker, L I G WorthleyAbstract:Objective To review the components of calcium, phosphate and Magnesium Metabolism that are relevant to the critically ill patient, in a two-part presentation. Data sources A review of articles reported on calcium, phosphate and Magnesium disorders in the critically ill patient. Summary of review Abnormal calcium Metabolism in the critically ill patient often presents with an alteration in plasma ionised calcium. The characteristic clinical features of an acute reduction in ionised plasma calcium include tetany, laryngospasm, paraesthesia, confusion, hallucinations, seizures and, rarely, hypotension all of which resolve with intravenous calcium administration. The clinical features of an acute increase in plasma ionised calcium include anorexia, nausea, vomiting, constipation, polyuria, weakness, lethargy, hypotonia and ectopic calcification and, depending on the aetiology, may require intravenous saline, frusemide, diphosphonate, glucocorticoid or calcitonin. Acute hypophosphataemia may present with paraesthasia, confusion, seizures, weakness, hypotension and heart failure and in the critically ill requires intravenous sodium or potassium phosphate. Hyperphosphataemia is often associated with renal failure and if severe usually presents with the clinical features of the associated hypocalcaemia. The clinical features of hypomagnesaemia include confusion, delerium, seizures, weakness, cramps, tetany and tachyarrhythmias, all of which resolve with intravenous Magnesium sulphate. Hypermagnesaemia is usually associated with excess Magnesium administration in a patient with renal failure and if severe can cause areflexia, hypotonia, respiratory and cardiac arrest. Intravenous calcium chloride will rapidly reverse the cardiovascular abnormalities. Conclusions Calcium, phosphate and Magnesium functions are closely linked with abnormal plasma levels of these compounds often causing similar cardiovascular and neurological features.
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the essentials of calcium Magnesium and phosphate Metabolism part i physiology
Critical Care and Resuscitation, 2002Co-Authors: S B Baker, L I G WorthleyAbstract:Objective To review the components of calcium, phosphate and Magnesium Metabolism that are relevant to the critically ill patient in a two-part presentation. Data sources A review of articles reported on calcium, phosphate and Magnesium disorders in the critically ill patient. Summary of review Calcium, phosphate and Magnesium have important intracellular and extracellular functions with their Metabolism often linked through common hormonal signals. A predominant portion of total body calcium is unionised within bone and serves an important structural function. Intracellular and extracellular ionised calcium changes are often linked and have important secretory and excitatory roles. The extracellular ionised calcium is carefully regulated by parathyroid hormone and vitamin D, whereas calcitonin is secreted largely in response to hypercalcaemia. Phosphorous is needed for bone structure although it also has an important role in cell wall structure, energy storage as ATP, oxygen transport and acid-base balance. Ionised calcium, in as far as it controls PTH secretion, indirectly controls urinary phosphate excretion. When plasma phosphate increases, tubular reabsorption also increases up to a maximum (TmPO4), thereafter phosphate is excreted. The minimum oral requirement for phosphate is about 20 mmol/day. Magnesium is a predominantly intracellular ion that acts as a metallo-coenzyme in more than 300 phosphate transfer reactions and thus has a critical role in the transfer, storage and utilisation of energy within the body. Extracellular Magnesium concentrations are largely controlled by the kidneys with the renal tubular maximum reabsorption (TmMg) controlling the plasma Magnesium concentration. Conclusions In the critically ill patient calcium, Magnesium and phosphate Metabolism, are often disturbed with an alteration in intake, increased liberation from bone and damaged tissue and reduced excretion (e.g. during renal failure), causing alterations in extracellular concentrations and subsequent disordered organ function.
Alan E Mckinnon - One of the best experts on this subject based on the ideXlab platform.
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a model of Magnesium Metabolism in young sheep transactions between plasma cerebrospinal fluid and bone
British Journal of Nutrition, 2004Co-Authors: Alexander B Robson, A R Sykes, Alan E Mckinnon, Stephen T BellAbstract:An extension of the previously proposed model of Mg Metabolism (Robson et al. 1997) has been developed to consider the transactions of Mg that are associated with cerebrospinal fluid (CSF) and bone. The representation of the CSF as a single Mg compartment with uptake from the plasma described by Michaelis‐ Menten kinetics gives very good agreement with published experiments. Analysis of the available information on resorption of Mg from adult bone indicates that this process makes a negligible contribution to Mg homeostasis and can be omitted from the model.
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a model of Magnesium Metabolism in young sheep Magnesium absorption and excretion
British Journal of Nutrition, 1997Co-Authors: Alexander B Robson, A C Field, A R Sykes, Alan E MckinnonAbstract:A model of Mg Metabolism in sheep is proposed. It is based on standard Michaelis-Menten enzyme kinetics to describe the transport of Mg across the rumen wall and passive diffusion to describe the absorption of Mg in the hindgut. Factors known to have an effect on Mg Metabolism in farm animals, namely the concentrations of K and Mg in the diet, and the physico-chemical conditions within the rumen as determined by the type of diet, are incorporated into the model. Consideration of the rumen as the only site of Mg absorption provided an inadequate mechanistic description of Mg Metabolism in sheep. To ensure compatibility between predicted Mg absorption and recent independent data sets for Mg balances, it was necessary to include in the model aspects of Mg absorption that operate in the hindgut. The results from this model suggest that there is a need for a series of experiments to determine the important aspects of Mg transport in the hindgut of sheep. Mechanisms of homeostasis are discussed.
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A model of Magnesium Metabolism in young sheep. Mg absorption and excretion. British Journal of Nutrition
1997Co-Authors: Alexander B Robson, A R Sykes, Alan E Mckinnon, Stephen T BellAbstract:extension of the previously proposed model of Mg Metabolism (Robson et al. 1997) has been developed to consider the transactions of Mg that are associated with cerebrospinal fluid (CSF) and bone. The representation of the CSF as a single Mg compartment with uptake from the plasma described by Michaelis–Menten kinetics gives very good agreement with published experiments. Analysis of the avail-able information on resorption of Mg from adult bone indicates that this process makes a negligible contribution to Mg homeostasis and can be omitted from the model. Magnesium: Mathematical modelling: Hypomagnesaemia: Grass tetany: Simulation Hypomagnesaemic tetany occurs in ruminant animals when the Mg concentration of the cerebrospinal fluid (CSF) falls below approximately 0·66 mmol/l (Meyer & Scholz, 1972). Normally the concentration of Mg in CSF is higher than that of plasma (Meyer & Scholz, 1972; Beal & Bligh, 1977). Bito (1969) and Oppelt et al. (1963) have demonstrated that an active transport mechan-ism is involved in transporting Mg from blood to CSF, and Oppelt et al. (1963) further showed that diffusion an
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A model of Magnesium Metabolism in young sheep. Magnesium absorption and excretion. Submitted to British Journal of Nutrition
1996Co-Authors: Alexander B Robson, A C Field, A R Sykes, Alan E MckinnonAbstract:A model of Mg Metabolism in sheep is proposed. It is based on standard Michaelis-Menten enzyme kinetics to describe the transport of Mg across the rumen wall and passive diffusion to describe the absorption of Mg in the hindgut. Factors known to have an effect on Mg Metabolism in farm animals, namely the concentrations of K and Mg in the diet, and the physico-chemical conditions within the rumen as determined by the type of diet, are incorporated into the model. Consideration of the rumen as the only site of Mg absorption provided an inadequate mechanistic description of Mg Metabolism in sheep. To ensure compatibility between predicted Mg absorption and recent independent data sets for Mg balances, it was necessary to include in the model aspects of Mg absorption that operate in the hindgut. The results from this model suggest that there is a need for a series of experiments to determine the important aspects of Mg transport in the hindgut of sheep. Mechanisms pf homeostasis are discussed. Magnesium: Mathematical modelling: Hypomagnesaemia: Grass tetany Hypomagnesaemia and the clinical deficiency hypomagnesaemic tetany, have been the focus of many studies during several decades (Wilson ef al. 1969; Wilcox & Hoff, 1974; Larvor, 1976). These have shown the importance of many confounding interaction
Mario Barbagallo - One of the best experts on this subject based on the ideXlab platform.
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Magnesium Metabolism in hypertension and type 2 diabetes mellitus
American Journal of Therapeutics, 2007Co-Authors: Mario Barbagallo, Ligia J Dominguez, Lawrence M ResnickAbstract:The increasing evidence for the clinical relevance of altered Magnesium Metabolism to states of altered insulin resistance confirms the role of Magnesium deficit as a possible underlying common mechanism of the "insulin resistance" of hypertension and altered glucose tolerance. The pioneer work of Lawrence M. Resnick and his group using the cellular ion-based approach that we are only partially presenting here has consistently contributed to the progress of the field, demonstrating (a) the critical importance of Magnesium Metabolism in regulating insulin sensitivity as well as vascular tone, and blood-pressure homeostasis; (b) that Magnesium deficiency, defined on the basis of intracellular free Magnesium levels, and or serum ionized Magnesium is a common feature of both diabetic and hypertensive states as well as various other cardiovascular and metabolic processes and aging; (c) the ability of environmental factors such as dietary nutrient-sugar and mineral content to alter the set point of steady-state cell ion activity; and (d) that Magnesium supplementation is indicated in conditions associated with Magnesium deficit although well-designed therapeutic trials of Magnesium in essential hypertension and type 2 diabetes mellitus are needed in the near future.
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Magnesium Metabolism in type 2 diabetes mellitus metabolic syndrome and insulin resistance
Archives of Biochemistry and Biophysics, 2007Co-Authors: Mario Barbagallo, Ligia J DominguezAbstract:Type 2 diabetes is characterized by cellular and extracellular Mg depletion. Epidemiologic studies showed a high prevalence of hypomagnesaemia and lower intracellular Mg concentrations in diabetic subjects. Insulin and glucose are important regulators of Mg Metabolism. Intracellular Mg plays a key role in regulating insulin action, insulin-mediated-glucose uptake and vascular tone. Reduced intracellular Mg concentrations result in a defective tyrosine-kinase activity, post-receptorial impairment in insulin action, and worsening of insulin resistance in diabetic patients. Mg deficit has been proposed as a possible underlying common mechanism of the "insulin resistance" of different metabolic conditions. Low dietary Mg intake is also related to the development of type 2 diabetes. Benefits of Mg supplementation on metabolic profile in diabetic subjects have been found in most, but not all clinical studies, and larger prospective studies are needed to support the potential role of dietary Mg supplementation as a possible public health strategy in diabetes risk.
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Magnesium Metabolism in insulin resistance metabolic syndrome and type 2 diabetes mellitus
2007Co-Authors: Mario Barbagallo, Ligia J Dominguez, Virna Brucato, Antonio Galioto, A Pineo, A Ferlisi, Ernesto Tranchina, Mario Belvedere, Ernesto Putignano, Giuseppe CostanzaAbstract:Magnesium plays a key role in regulating insulin action, insulin-mediated glucose uptake, and vascular tone. Intracellular Magnesium depletion may result in a defective tyrosine—kinase activity at the insulin receptor level, in a postreceptorial impairment in insulin action, and clinically in a worsening of insulin resistance. Intra- and extracellular alterations of Magnesium Metabolism have been identified in clinical states characterized by insulin resistance, such as metabolic syndrome, hypertension, altered glucose tolerance, type 2 diabetes, and aging. Several studies, from our and other’s groups, have confi rmed the clinical relevance of alterations of Magnesium homeostasis in these conditions and have highlighted the importance of an accurate definition of the Magnesium status. While measurements of total serum Magnesium levels have been proven inadequate for this purpose because important Magnesium depletions are required before total serum level decreases, two technologies, 31P nuclear magnetic resonance (31P-NMR) spectroscopy and Magnesium-specifi c ion-selective electrodes, that, respectively, measure intracellular and extracellular free levels of Magnesium, have a higher sensitivity in detecting Magnesium deficits. A number of evidences have confirmed that Magnesium supplementation is indicated in conditions associated with Magnesium deficit, although well-designed therapeutic trials with oral Magnesium supplements to study the beneficial effects in metabolic syndrome and in type 2 diabetes are needed.
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cellular free Magnesium depletion in brain and muscle of normal and preeclamptic pregnancy a nuclear magnetic resonance spectroscopic study
Hypertension, 2004Co-Authors: Lawrence M Resnick, Mordechai Bardicef, Orit Bardicef, Yoram Sorokin, Mario Barbagallo, Jeffrey L Evelhoch, Ligia J Dominguez, Brian A Mason, David B CottonAbstract:Preeclampsia is a pregnancy disorder of unknown origin, characterized by vasospasm, elevated blood pressure, and increased neuromuscular irritability, features common to syndromes of Magnesium deficiency. Evidence of serum and ionized Magnesium Metabolism disturbances have been observed in women with preeclampsia. This and the therapeutic utility of Magnesium in preeclampsia led us to investigate the extent to which an endogenous tissue Magnesium deficiency might be present in and contribute to its pathophysiology. We used (31)P nuclear magnetic resonance spectroscopy to noninvasively measure in situ intracellular-free Magnesium levels in brain and skeletal muscle of fasting nonpregnant women (n=12), and of third trimester women with uncomplicated pregnancies (n=11) and preeclampsia (n=7). Compared with nonpregnant controls (brain 519+/-59 micromol/L; muscle 604+/-34 micromol/L), brain and skeletal muscle intracellular Magnesium levels were significantly lower in both normal pregnant (brain 342+/-23 micromol/L; muscle 482+/-40 micromol/L; P=0.05 for both tissues) and preeclamptic women (brain 229+/-17 micromol/L; muscle 433+/-46 micromol/L; P=0.05 for both tissues). Brain intracellular Magnesium was further reduced in preeclamptics compared with normal pregnant subjects (P=0.05). For all pregnant subjects, blood pressure was significantly and inversely related to the concomitantly measured intracellular Magnesium level in brain (systolic, r=-0.59, P=0.01; diastolic, r=-0.52, P=0.02) but not in muscle. Cellular Magnesium depletion is characteristic of normal pregnancy and may be one factor contributing to the pathophysiology of preeclampsia. Furthermore, the influence of central nervous system factors on blood pressure may be mediated, at least in part, by ambient intracellular Magnesium levels.
