There are two studies on this page!!
Overview Diabetes and vitamin D contains the following summary
- Diabetes is 5X more frequent far from the equator
- Children getting 2,000 IU of vitamin D are 8X less likely to get Type 1 diabetes
- Obese people get less sun / Vitamin D - and also vitamin D gets lost in fat
- Sedentary people get less sun / Vitamin D
- Worldwide Diabetes increase has been concurrent with vitamin D decrease and air conditioning
- Elderly get 4X less vitamin D from the same amount of sun
Elderly also spend less time outdoors and have more clothes on
- All items in category Diabetes and Vitamin D
480 items: both Type 1 and Type 2
Vitamin D appears to both prevent and treat diabetes
- Appears that >2,000 IU will Prevent
- Appears that >4,000 IU will Treat , but not cure
- Appears that Calcium and Magnesium are needed for both Prevention and Treatment
- which are just some of the vitamin D cofactors
Number of articles in both categories of Diabetes and:
- Dark Skin
23 ; Intervention 52 ; Meta-analysis 34 ; Obesity 28 ; Pregnancy 40 ; T1 (child) 37 ; Omega-3 11 ; Vitamin D Receptor 21 ; Genetics 11 ; Magnesium 19 Click here to see details 480 items along with related searches
Pages listed in BOTH the categories Diabetes and Magnesium
- Excessive insulin decreases vitamin D in 4 ways – problems for diabetic COVID-19 – Dec 2020
- Low Magnesium associated with diabetes, etc. – meta-analysis 2016
- Low Level Laser Therapy greatly increased Vitamin D and Magnesium (for diabetics with nephropathy) – March 2019
- Young Diabetics had 3.8 X higher risk of Parkinson’s (perhaps low Mg or low Vitamin D)– June 2018
- Cardiometaboic problems decreased with increased Vitamin D, unless low Magnesium – Aug 2017
- Diabetes 29 % less likely if consume lots of Magnesium and cereal fiber (surveys of 200,000 people) – Oct 2017
- Magnesium is associated with prevention and treatment of Diabetes – Meta-analysis Aug 2016
- Type 2 diabetes associated with low Magnesium
- MAGNESIUM IN MAN - IMPLICATIONS FOR HEALTH AND DISEASE – review 2015
- More vitamin D makes for better health – dissertation based on Rotterdam studies – Oct 2015
- Prediabetes reduced in half by those getting Magnesium Chloride – RCT April 2015
- Type II Diabetes might be prevented and treated with Magnesium – Review Feb 2015
- Diabetes decreased with 300 mg of Mg (Mg Sulfate) – RCT July 2014
- Daily Magnesium improved all aspects of metabolic profile – RCT July 2014
- Diabetes and low Magnesium - Mercola 2014 - 2019
- Diabetics have problems with low Magnesium, especially if taking statins – Aug 2013
- Low Magnesium and type II diabetes – June 2012
- Hypothesis: Decreasing Magnesium and increasing CaMg ratio are increasing health problems – 2012 - 2013
- Reduced chance of diabetes 46 percent with Magnesium - Oct 2010
Table of contents
- Magnesium and Type 2 Diabetes: An Update
- Diabetes treated with 382 mg Magnesium ( 30 mg of MgCl) RCT April 2015
International Journal of Diabetes and Clinical Research
Mario Barbagallo* and Ligia J. Dominguez
Geriatric Unit, Department of Internal Medicine and Medical Specialties (DIMIS), University of Palermo, Italy
‘Corresponding author: Mario Barbagallo, MD, PhD, Geriatric Unit, Department of Internal Medicine and Medical Specialties (DIMIS), University of Palermo, Via del Vespro 129, 90127 Palermo, Italy, Tel: 0039-091-6552885, Fax: 0039-091-6552952, E-mail: mario.barbagallo at unipa.it
The link between magnesium (Mg) deficiency and type 2 diabetes mellitus is well known. Type 2 diabetes is frequently associated with both extracellular and intracellular Mg deficits. A chronic latent Mg deficit or an overt clinical hypomagnesaemia is common in subjects with type 2 diabetes, especially in those with poorly controlled glycemic profiles. 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, postreceptorial impairment in insulin action and worsening of insulin resistance in diabetic patients. A low Mg intake and an increased Mg urinary loss appear the most important mechanisms that may favor Mg depletion in patients with type 2 diabetes. Low dietary Mg intake has been related to the development of type 2 diabetes and metabolic syndrome. 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.
The objective of this review is to revise current evidences on the mechanisms of Mg deficiency in diabetes mellitus type 2 and on the possible role of Mg supplementation in the prevention and management of the disease.
Magnesium (Mg) is the fourth most abundant mineral present in the human body and the second intracellular cation in living cells after potassium. Most Mg located in the human adult’s body is distributed in the intracellular compartment (99%), and only 1% in the extracellular fluid . The link between Mg deficiency and type 2 diabetes mellitus is well known. Type 2 diabetes is frequently associated with both extracellular and intracellular Mg depletion. Several epidemiologic studies have recognized a high prevalence of hypomagnesaemia in subjects with type 2 diabetes, especially in those with poorly controlled glycemic profiles, with longer duration of the disease and with the presence of micro-macrovascular chronic complications [2-6].
The definition of Mg deficiency seems simpler than it is, primarily because accurate clinical tests for the assessment of Mg status are lacking. Patients are considered frank hypomagnesaemic with serum Mg concentrations <0.61mmol/L or 1.5mg/dL [7-9]. Mg concentrations <0.75mmol/L or 1.8mg/dL may be considered a preclinical hypomagnesaemia [10,11].
Because of the lack of sensitivity of total serum Mg, a Mg deficiency can be present without hypomagnesaemia. However, hypomagnesaemia is usually indicative of a systemic Mg deficit. Depletion in intracellular and serum ionized Mg can be found in many subjects with total serum Mg still in the normal range . We have recently confirmed that diabetic older patients are more prone to hypomagnesaemia; this condition being closely related with metabolic control as measured by glycated hemoglobin even after adjustment for relevant confounders. Ionized Mg may help to identify older diabetic adults with low concentrations of blood Mg that are not evident with the only measurement of total Mg .
At the cellular level, cytosolic free Mg levels are consistently reduced in subjects with type 2 diabetes mellitus, when compared with nondiabetic subjects [1,13,14]. An impairment of cellular Mg uptake mechanism, and a the decrease in the cellular ATP level, may contribute, at least in part, to explain the decrease in cellular Mg content observed under diabetic conditions . The relationship between intra-cellular Mg and ATP concentration is rather complex. The decrease in cellular ATP might partially explain the decrease in cellular Mg. Otherwise, a decrease in cellular ATP leads to a decreased binding of Mg to ATP in the formation of MgATP which might increase the intracellular Mg concentration.
The objective of this review is to revise current evidences on the mechanisms of Mg deficiency in diabetes mellitus type 2 and on the possible role of Mg supplementation in the prevention and management of the disease.
A low Mg intake and an increased Mg urinary loss appears the most important mechanisms that may favor Mg depletion in patients
with type 2 diabetes, while Mg absorption and retention of dietary Mg seems not to be impaired in patients with type 2 diabetes [1,16,17]. With regard to low Mg intake, changes in dietary habits in the western world have resulted in daily Mg intake close to, or even below, the recommended daily allowances. The ARIC study demonstrated a relationship between serum Mg and the development of diabetes in the general population . Diabetes is associated with renal calcium and Mg wasting [19-21], but the molecular mechanism(s) of these defects are not completely elucidated . Recent findings in obese diabetic rats found that TRPM6 was down regulated explaining renal Mg wasting . The findings from Man don, showing a insulin- induced Mg uptake in the thick ascending loop of Henle may also have a role , since hyperinsulinemia and insulin resistance may lead to a decreased Mg uptake, and an increase Mg excretion. Hyperglycemia also contributes to an increased urinary Mg wasting contributing to Mg depletion. Plasma Mg levels were found inversely correlated with the urinary Mg excretion rate and with fasting blood glucose values, suggesting that the tubular reabsorption of Mg is decreased in presence of severe hyperglycemia .
An increased renal Mg transporter abundance was found in diabetic rats and may represent a compensatory adaptation for the increased load of Mg to the distal tubule. Insulin administration completely corrected the hyperglycemia-associated hypercalciuria and hypermagnesiuria, and reversed the increase of Mg transporter abundance . An improved metabolic control was associated with reduced urinary Mg losses . Hyperinsulinemia, which is present in insulin resistant states, may contribute per se to the urinary Mg depletion, to the reduced sensitivity to insulin, and may itself affect Mg transport . Djurhuus in healthy volunteers with hyperinsulinemia suggested that in these people is different from hyperinsulinemia in people with prediabetes, metabolic syndrome [20,25].
In addition other factors like metabolic acidosis or hypoalbuminemia also seem to affect renal Mg wasting in diabetes . The use of loop and thiazide diuretics, often prescribed in diabetic patients with hypertension and/or cardiovascular diseases, also promote Mg wasting.
Mg deficiency in type 2 diabetes may take the form of a chronic latent Mg deficit rather than an overt clinical hypomagnesaemia , and may have clinical importance because the Mg ion is a crucial cofactor for many enzymatic reactions involved in a myriad of metabolic processes. The Mg ion plays a key role in the regulation of the effects of insulin and insulin-mediated cellular glucose intake. Mg is a necessary co-factor in >300 enzymatic reactions that include all the enzymes determinant of glycolysis. Intracellular Mg is a critical cofactor for enzymes involved in carbohydrate metabolism, and specifically in the process of phosphorylation of the tyrosine-kinase of the insulin receptor as well as all other protein kinases in the insulin signaling, and all ATP and phosphate transfer-associated enzymes, such as the CaATPases in the plasma membrane and the endoplasmic reticulum [1,26].
Mg deficiency may result in disorders of tyrosine kinase activity of the insulin receptor, event related to the development of post-receptorial insulin resistance and decreased cellular glucose utilization, that is, the lower the basal Mg, the greater the amount of insulin required to metabolize the same glucose load, indicating a decreased insulin sensitivity . Cellular concentrations of Mg are in the 100-300nmol/L range, which is close to the dissociation constant of many enzymes systems using ATP or phosphate transference, confirming the clinical importance of Mg deficiency. A deficient Mg status may be a secondary consequence or may precede and cause insulin resistance and altered glucose tolerance, and even diabetes. Inflammation and oxidative stress have been proposed to be a possible link between Mg deficit and insulin resistance/metabolic syndrome. Chronic hypomagnesaemia and conditions commonly associated with Mg deficiency, such as type 2 diabetes mellitus, metabolic syndrome and aging, are associated with increased free radical formation and subsequent damage to cellular processes [27,28]. Aging is frequently associated with insulin resistance and glucose intolerance. A continuous age-dependent fall of intracellular Mg levels in peripheral blood cells of healthy elderly subjects is present, these alterations being indistinguishable from those occurring, independently of age, in essential hypertension or type 2 diabetes [14,28].
The relevance of altered cellular Mg metabolism to tissutal insulin sensitivity suggest a possible role of Mg in contributing to the clinical coincidence of Mg depletion to clinical conditions of insulin resistance such as hypertension, metabolic syndrome, type 2 diabetes as well with the increased incidence of each of these conditions with age, a condition itself characterized by a tendency to Mg depletion .
Altogether, independent to the cause of poor plasma and intracellular Mg content, a depletion of Mg seems to contribute to an impairment of insulin sensitivity. A deficient Mg status may not just be a secondary consequence of type 2 diabetes but may precedes and contributes itself to the development of insulin resistance and altered glucose tolerance, and even type 2 diabetes. We have suggested a role for Mg deficit as a possible unifying mechanism of conditions associated to “insulin resistance, including type 2 diabetes mellitus, metabolic syndrome, and essential hypertension [1,17]. The Mg deficit could precede and cause post-receptorial resistance of insulin and alter the glucose tolerance.
It has been suggested that Mg deficiency may be a factor implicated in the pathogenesis of diabetes complications. Cellular ionic alterations are related to the cardiovascular structural modifications often present in diabetes. A significant relation was found between fasting levels of intracellular Mg levels and cardiovascular structural indices . In type 2 diabetic subjects, even in the absence of elevated blood pressure, suppressed intracellular Mg levels are associated with cardiac hypertrophy, and specifically with increased echocardiographically measured posterior wall thickness and left ventricular mass index in both diabetic and/or hypertensive subjects . Similarly, aortic distensibility values determined by magnetic resonance imaging in normal and hypertensive humans were closely and positively related to concomitantly measured levels of cellular Mg measured in situ in brain and skeletal muscle tissue by 31P-NMR magnetic resonance spectroscopic techniques: the more suppressed the intracellular Mg, the stiffer (less distensible) the aorta . Low serum Mg concentrations are associated with a high prevalence of premature ventricular complexes in obese adults with type 2 diabetes . In patients with type 2 diabetes mellitus, low circulating Mg levels have been associated also with a more rapid decline of renal function. Hypomagnesaemia is currently considered an accurate predictor of progression to end stage renal disease and death and in patients with type 2 diabetic nephropathy [31-33]. A Mg deficit have been associated to cognitive decline , multimorbidity  and aging [28,36].
The hypothesis that Mg deficit in the diet would induce and/or exacerbate insulin resistance is confirmed by data, both in humans and in experimental animals, which have consistently shown dietary Mg deficiency is associated to insulin resistance [37-43]. Mg- deficient diet in sheep cause a significant impairment of insulin- mediated glucose uptake  and Mg supplementation delayed the development of diabetes in a rat model of diabetes . Higher Mg intake is associated with lower fasting insulin concentrations among women without diabetes , and a significant negative correlation is present between total dietary Mg intake and the insulin responses to an oral glucose tolerance test . Rats fed a low Mg diet showed a significant increase in blood glucose and triglyceride levels . Suarez et al. investigated the effect of dietary-induced Mg deficiency on glucose disposal, glucose-stimulated insulin secretion and insulin action on skeletal muscle in rats, which were fed a low Mg-containing diet. Mg depletion provoked a deleterious effect on glucose metabolism due to an impairment of both insulin secretion and action. In rats, maternal Mg restriction induces insulin resistance in pups by 6 months of age, whereas additional perinatal Mg deficiency impairs glucose tolerance . The insulin resistance observed in skeletal muscle of Mg-deficient rats was linked, at least in part, to a defective tyrosine kinase activity of insulin receptors .
Dietary Mg deficits have also been associated to the development of diabetes. Deficiencies of Mg status including both hypomagnesaemia and/or reduced dietary Mg intake have been associated with an increased risk to develop glucose intolerance and diabetes [18,45-47] while an increased Mg intake is associated with a significant decline in the incidence of type 2 diabetes .
Various epidemiological studies have confirmed a clear and direct relationship between the Mg status in the diet, type 2 diabetes and metabolic syndrome, suggesting that the higher consumption of Mg is related with a reduction of the incidence of these conditions. Two meta-analyses of prospective studies concluded that Mg intake is inversely associated with type 2 diabetes [49,50]. Mg intake has been also strongly and inversely associated with the metabolic syndrome [37,51], while hypomagnesaemia has been independently associated with the development of impaired glucose tolerance . Increased Mg intake is associated with increased insulin sensitivity  and a decreased risk of developing type 2 diabetes [54,55]. In a prospective study of more than 85,000 women, followed for 18 months the relative risk of developing type 2 diabetes for women in the highest quintile of Mg consumption was 0.68 compared with women in the lowest quintile after adjustment for a number of potentially confounding variables. A significant inverse association was found between Mg intake and diabetes risk . In the Women's Health Study, a cohort of 39,345 U.S. women aged >45 years with no previous history of cardiovascular disease, cancer, or type 2 diabetes was recruited and followed for an average of 6 years. A significant inverse association was found between Mg intake and the risk of developing type 2 diabetes, supporting a protective role of higher intake of Mg in reducing the risk of developing type 2 diabetes .
In a large cohort of young American adults, participating in the Coronary Artery Risk Development in Young Adults (CARDIA) study, during the 20-year follow-up, Mg intake was inversely longitudinally associated with the incidence of diabetes in this young American population, after adjustment for potential confounders. This inverse association may be explained, at least in part, by the inverse correlations of Mg intake with systemic inflammation and insulin resistance .
Hypomagnesemia has been associated with inflammation and increased production of free oxygen radicals [57,58]. Poor Mg status may trigger the development of a proinflammatory state both by causing excessive production and release of interleukins and by elevating circulating concentrations of proinflammatory neuropeptides that trigger activation of low-grade chronic inflammation [28,59]. Thus, dietary-induced Mg deficiency increases thromboxane urinary concentration and enhances angiotensin- induced aldosterone synthesis. These effects are associated with a decrease in insulin action, further confirming that Mg deficiency may be a common factor associated with insulin resistance and vascular disease .
The detection and correction of altered Mg status in diabetic patients is clinically appropriate, although many physicians tend to ignore Mg status. The increased risks to develop glucose intolerance and type 2 diabetes mellitus in subjects with dietary and/or serum Mg deficits have suggested potential benefits of Mg supplementation in persons who have type 2 diabetes or risk factors for diabetes. The use of Mg supplements has also been proposed as a potential tool for the prevention and the metabolic control of type 2 diabetes [61,62].
Benefits of Mg supplements on glycemic profile in most but not all studies explain whether according to meta-analysis a net beneficial effect is to be expected. The clinical evidences of a clear effects of Mg supplements on the metabolic profile of diabetic subjects are controversial, benefits having been found in many [8,61,63,64], but not in all clinical studies .
While the body of evidence from epidemiological studies consistently shows a strong inverse relationship between dietary Mg intake and the risk of developing type 2 diabetes mellitus, results from clinical trials are scarce and controversial . Still, the risk of residual confounding factors in these kinds of analyses deserves to be taken into consideration. The hypothesis of a role of supplemental Mg in the control of type 2 diabetes still needs to be confirmed by specific and well-designed large randomized clinical trials with Mg [67,68].
Mg supplementation may improve glycemic concentrations in fasting and postprandial states and improves the insulin-mediated glucose uptake measured by euglycemic insulin clamp, with a significant relationship between the parallel increase in plasma and erythrocyte Mg concentration and the progressive increase in insulin sensitivity . Mg supplementation was also able to restore altered endothelial function in elderly diabetic subjects , and was suggested to be useful in the treatment of depression in the elderly with type 2 diabetes and hypomagnesaemia .
Mooren et al. in normomagnesemic insulin resistant subjects, Mg improved fasting glycemia . Presumably, the main problem is that all RCT were underpowered, partially through overestimation of the treatment effect. Differences may be related to the fact that most of the existing studies have included a small number of subjects, using different Mg doses and different Mg salts.
The available studies have shown that Mg may mediate the favorable impact of whole grains on insulin sensitivity cereal on insulin sensitivity [73-76]. A recent clinical randomized double-blind placebo-controlled trial has shown that oral Mg supplementation decreases C-reactive protein levels in subjects with prediabetes and frank hypomagnesaemia . In type 2 diabetic patients with clinical hypomagnesaemia (index of an already advanced Mg deficit) oral Mg supplementation had beneficial effects on fasting and postprandial glucose levels and on insulin sensitivity . A small but significant beneficial effect of Mg supplements on insulin sensitivity among nondiabetic, apparently healthy subjects was suggested . Altogether, Mg supplementation in diabetic patients (with frank Mg deficiency) corrects the deficit in intracellular free Mg levels, improves insulin sensitivity, and may protect against diabetic complications. The positive effects of a high intake of Mg on systemic inflammation and insulin resistance may help to explain at least some of its favorable effects.
We suggest that fact that most but not all diabetic subjects have a Mg deficiency and that no large clinical trial have been specifically focused on subjects with a Mg deficit, diagnosed with an accurate and reliable technique, may help to explain the discrepancy between the unclear role of supplemental Mg on glycemic control in diabetics, and the significant impact on diabetes risk in prospective epidemiologic studies.
Differences in baseline Mg status and metabolic control, and age of the subjects are other potential factors that may help to explain the differences among the studies. Future prospective randomized large clinical studies are needed to support the potential role of dietary Mg supplementation as a possible public health strategy to reduce diabetes risk in the population.
- Barbagallo M, Dominguez LJ (2007) Magnesium metabolism in type 2 diabetes mellitus, metabolic syndrome and insulin resistance. Arch Biochem Biophys 458: 40-47.
- Mather HM, Levin GE (1979) Magnesium status in diabetes. Lancet 1: 924.
- Schnack C, Bauer I, Pregant P, Hopmeier P, Schernthaner G (1992) Hypomagnesaemia in type 2 (non-insulin-dependent) diabetes mellitus is not corrected by improvement of long-term metabolic control. Diabetologia 35: 77-79.
- Ramadass S, Basu S, Srinivasan AR (2015) SERUM magnesium levels as an indicator of status of Diabetes Mellitus type 2. Diabetes Metab Syndr 9: 42-45.
- Ma J, Folsom AR, Melnick SL, Eckfeldt JH, Sharrett AR, et al. (1995) Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin, and carotid arterial wall thickness: the ARIC study. Atherosclerosis Risk in Communities Study. J Clin Epidemiol 48: 927940.
- Del Gobbo LC, Song Y, Poirier P, Dewailly E, Elin RJ, et al. (2012) Low serum magnesium concentrations are associated with a high prevalence of premature ventricular complexes in obese adults with type 2 diabetes. Cardiovasc Diabetol 11: 23.
- Hashizume N, Mori M (1990) An analysis of hypermagnesemia and hypomagnesemia. Jpn J Med 29: 368-372.
- Guerrero-Romero F, Tamez-Perez HE, Gonzalez-Gonzalez G, Salinas- Martmez AM, Montes-Villarreal J, et al. (2004) Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. Diabetes Metab 30: 253-258.
- Wong ET, Rude RK, Singer FR, Shaw ST Jr (1983) A high prevalence of hypomagnesemia and hypermagnesemia in hospitalized patients. Am J Clin Pathol 79: 348-352.
- Chernow B, Bamberger S, Stoiko M, Vadnais M, Mills S, et al. (1989) Hypomagnesemia in patients in postoperative intensive care. Chest 95: 391397.
- Whang R, Ryder KW (1990) Frequency of hypomagnesemia and hypermagnesemia. Requested vs routine. JAMA 263: 3063-3064.
- Barbagallo M, Di Bella G, Brucato V, D'Angelo D, Damiani P, et al. (2014) Serum ionized magnesium in diabetic older persons. Metabolism 63: 502509.
- Resnick LM, Altura BT, Gupta RK, Laragh JH, Alderman MH, et al. (1993) Intracellular and extracellular magnesium depletion in type 2 (non-insulin- dependent) diabetes mellitus. Diabetologia 36: 767-770.
- Barbagallo M, Gupta RK, Dominguez LJ, Resnick LM (2000) Cellular ionic alterations with age: relation to hypertension and diabetes. J Am Geriatr Soc 48: 1111-1116.
- Barbagallo M, Dominguez LJ, Resnick LM (2007) Magnesium metabolism in hypertension and type 2 diabetes mellitus. Am J Ther 14: 375-385.
- Walti MK, Zimmermann MB, Walczyk T, Spinas GA, Hurrell RF (2003) Measurement of magnesium absorption and retention in type 2 diabetic patients with the use of stable isotopes. Am J Clin Nutr 78: 448-453.
- Barbagallo M, Dominguez LJ, Galioto A, Ferlisi A, Cani C, et al. (2003) Role of magnesium in insulin action, diabetes and cardio-metabolic syndrome X. Mol Aspects Med 24: 39-52.
- Kao WH, Folsom AR, Nieto FJ, Mo JP, Watson RL, et al. (1999) Serum and dietary magnesium and the risk for type 2 diabetes mellitus: the Atherosclerosis Risk in Communities Study. Arch Intern Med 159: 2151-2159.
- McNair P, Christensen MS, Christiansen C, Madsbad S, Transb0l I (1982) Renal hypomagnesaemia in human diabetes mellitus: its relation to glucose homeostasis. Eur J Clin Invest 12: 81-85.
- Djurhuus MS, Sk0tt P, Hother-Nielson O, Klitgaard NA, Beck-Nielsen H (1995) Insulin increases renal magnesium excretion: a possible cause of magnesium depletion in hyperinsulinaemic states. Diabet Med 12: 664-669.
- Pham PC, Pham PM, Pham SV, Miller JM, Pham PT (2007) Hypomagnesemia in patients with type 2 diabetes. Clin J Am Soc Nephrol 2: 366-373.
- Lee CT, Lien YH, Lai LW, Chen JB, Lin CR, et al. (2006) Increased renal calcium and magnesium transporter abundance in streptozotocin-induced diabetes mellitus. Kidney Int 69: 1786-1791.
- Takayanagi K, Shimizu T, Tayama Y, Ikari A, Anzai N, et al. (2014) Down- regulation of transient receptor potential (TRP) M6 channel as a cause of hypermagnesiuric hypomagnesemia in obese type-2 diabetic rats. Am J Physiol Renal Physiol: ajprenal 00593 02013.
- Mandon B, Siga E, Chabardes D, Firsov D, Roinel N, et al. (1993) Insulin stimulates Na+, Cl-, Ca2+, and Mg2+ transports in TAL of mouse nephron: cross-potentiation with AVP. Am J Physiol 265: F361-369.
- Djurhuus MS (2001) New data on the mechanisms of hypermagnesuria in type I diabetes mellitus. Magnes Res 14: 217-223.
- Saris NE, Mervaala E, Karppanen H, Khawaja JA, Lewenstam A (2000) Magnesium. An update on physiological, clinical and analytical aspects. Clin Chim Acta 294: 1-26.
- Weglicki WB (2012) Hypomagnesemia and inflammation: clinical and basic aspects. Annu Rev Nutr 32: 55-71.
- Barbagallo M, Dominguez LJ (2010) Magnesium and aging. Curr Pharm Des 16: 832-839.
- Barbagallo M, Gupta RK, Resnick LM (1996) Cellular ions in NIDDM: relation of calcium to hyperglycemia and cardiac mass. Diabetes Care 19: 1393-1398.
- Resnick LM, Militianu D, Cunnings AJ, Pipe JG, Evelhoch JL, et al. (1997). Direct magnetic resonance determination of aortic distensibility in essential hypertension: relation to age, abdominal visceral fat, and in situ intracellular free magnesium. Hypertension 30: 654-659.
- Sakaguchi Y, Shoji T, Hayashi T, Suzuki A, Shimizu M, et al. (2012) Hypomagnesemia in type 2 diabetic nephropathy: a novel predictor of end- stage renal disease. Diabetes Care 35: 1591-1597.
- Van Laecke S, Nagler EV, Verbeke F, Van Biesen W, Vanholder R (2013) Hypomagnesemia and the risk of death and GFR decline in chronic kidney disease. Am J Med 126: 825-831.
- Tin A, Grams ME, Maruthur NM, Astor BC, Couper D, et al. (2014) Results from the Atherosclerosis Risk in Communities study suggest that low serum magnesium is associated with incident kidney disease. Kidney Int: doi: 10.1038/ki.2014.331. [Epub ahead of print]
- Barbagallo M, Belvedere M, Di Bella G, Dominguez LJ (2011) Altered ionized magnesium levels in mild-to-moderate Alzheimer's disease. Magnesium research: official organ of the International Society for the Development of Research on Magnesium 24: S115-121.
- Ruel G, Shi Z, Zhen S, Zuo H, Kroger E, et al. (2014) Association between nutrition and the evolution of multimorbidity: the importance of fruits and vegetables and whole grain products. Clin Nutr 33: 513-520.
- Barbagallo M, Belvedere M, Dominguez LJ (2009) Magnesium homeostasis and aging. Magnes Res 22: 235-246.
- He K, Liu K, Daviglus ML, Morris SJ, Loria CM, et al. (2006) Magnesium intake and incidence of metabolic syndrome among young adults. Circulation 113: 1675-1682.
- Matsunobu S, Terashima Y, Senshu T, Sano H, Itoh H (1990) Insulin secretion and glucose uptake in hypomagnesemic sheep fed a low magnesium, high potassium diet. J Nutr Biochem 1: 167-171.
- Balon TW, Gu JL, Tokuyama Y, Jasman AP, Nadler JL (1995) Magnesium supplementation reduces development of diabetes in a rat model of spontaneous NIDDM. Am J Physiol 269: E745-752.
- Fung TT, Manson JE, Solomon CG, Liu S, Willett WC, et al. (2003) The association between magnesium intake and fasting insulin concentration in healthy middle-aged women. J Am Coll Nutr 22: 533-538.
- Humphries S, Kushner H, Falkner B (1999) Low dietary magnesium is associated with insulin resistance in a sample of young, nondiabetic Black Americans. Am J Hypertens 12: 747-756.
- Chaudhary DP, Boparai RK, Sharma R, Bansal DD (2004) Studies on the development of an insulin resistant rat model by chronic feeding of low magnesium high sucrose diet. Magnes Res 17: 293-300.
- Venu L, Kishore YD, Raghunath M (2005) Maternal and perinatal magnesium restriction predisposes rat pups to insulin resistance and glucose intolerance. J Nutr 135: 1353-1358.
- Suarez A, Pulido N, Casla A, Casanova B, Arrieta FJ, et al. (1995) Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats. Diabetologia 38: 1262-1270.
- Mather HM, Nisbet JA, Burton GH, Poston GJ, Bland JM, et al. (1979) Hypomagnesaemia in diabetes. Clin Chim Acta 95: 235-242.
- Yokota K (2005) [Diabetes mellitus and magnesium]. Clin Calcium 15: 203212.
- Longstreet DA, Heath DL, Vink R (2005) A potential link between magnesium intake and diabetes in Indigenous Australians. Med J Aust 183: 219-220.
- Colditz GA, Manson JE, Stampfer MJ, Rosner B, Willett WC, et al. (1992) Diet and risk of clinical diabetes in women. Am J Clin Nutr 55: 1018-1023.
- Larsson SC, Wolk A (2007) Magnesium intake and risk of type 2 diabetes: a meta-analysis. J Intern Med 262: 208-214.
- Dong JY, Qin LQ (2012) Dietary calcium intake and risk of type 2 diabetes: possible confounding by magnesium. Eur J Clin Nutr 66: 408-410.
- Song Y, Ridker PM, Manson JE, Cook NR, Buring JE, et al. (2005) Magnesium intake, C-reactive protein, and the prevalence of metabolic syndrome in middle-aged and older U.S. women. Diabetes Care 28: 1438-1444.
- Guerrero-Romero F, Rascon-Pacheco RA, Rodnguez-Moran M, de la Pena JE, Wacher N (2008) Hypomagnesaemia and risk for metabolic glucose disorders: a 10-year follow-up study. Eur J Clin Invest 38: 389-396.
- Ma B, Lawson AB, Liese AD, Bell RA, Mayer-Davis EJ (2006) Dairy, magnesium, and calcium intake in relation to insulin sensitivity: approaches to modeling a dose-dependent association. Am J Epidemiol 164: 449-458.
- Song Y, Manson JE, Buring JE, Liu S (2004) Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women. Diabetes Care 27: 59-65.
- Lopez-Ridaura R, Willett WC, Rimm EB, Liu S, Stampfer MJ, et al. (2004) Magnesium intake and risk of type 2 diabetes in men and women. Diabetes Care 27: 134-140.
- Kim DJ, Xun P, Liu K, Loria C, Yokota K, et al. (2010) Magnesium intake in relation to systemic inflammation, insulin resistance, and the incidence of diabetes. Diabetes Care 33: 2604-2610.
- Rock E, Astier C, Lab C, Vignon X, Gueux E, et al. (1995) Dietary magnesium deficiency in rats enhances free radical production in skeletal muscle. J Nutr 125: 1205-1210.
- Malpuech-Brugere C, Nowacki W, Daveau M, Gueux E, Linard C, et al. (2000) Inflammatory response following acute magnesium deficiency in the rat. Biochim Biophys Acta 1501: 91-98.
- Guerrero-Romero F, Rodriguez-Moran M (2006) Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome. Diabetes Metab Res Rev 22: 471-476.
- Nadler JL, Buchanan T, Natarajan R, Antonipillai I, Bergman R, et al. (1993) Magnesium deficiency produces insulin resistance and increased thromboxane synthesis. Hypertension 21: 1024-1029.
- Guerrero-Romero F, Rodriguez-Moran M (2005) Complementary therapies for diabetes: the case for chromium, magnesium, and antioxidants. Arch Med Res 36: 250-257.
- McCarty MF (1996) Complementary vascular-protective actions of magnesium and taurine: a rationale for magnesium taurate. Med Hypotheses 46: 89-100.
- Rodriguez-Moran M, Guerrero-Romero F (2003) Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial. Diabetes Care 26: 1147-1152.
- Yokota K, Kato M, Lister F, li H, Hayakawa T, et al. (2004) Clinical efficacy of magnesium supplementation in patients with type 2 diabetes. J Am Coll Nutr 23: 506S-509S.
- de Valk HW, Verkaaik R, van Rijn HJ, Geerdink RA, Struyvenberg A (1998) Oral magnesium supplementation in insulin-requiring Type 2 diabetic patients. Diabet Med 15: 503-507.
- Rodriguez-Moran M, Simental Mendia LE, Zambrano Galvan G, Guerrero- Romero F (2011) The role of magnesium in type 2 diabetes: a brief based- clinical review. Magnesium research: official organ of the International Society for the Development of Research on Magnesium 24: 156-162.
- McCarty MF (2005) Nutraceutical resources for diabetes prevention--an update. Med Hypotheses 64: 151-158.
- Schulze MB, Hu FB (2005) Primary prevention of diabetes: what can be done and how much can be prevented? Annu Rev Public Health 26: 445-467.
- Paolisso G, Barbagallo M (1997) Hypertension, diabetes mellitus, and insulin resistance: the role of intracellular magnesium. Am J Hypertens 10: 346-355.
- Barbagallo M, Dominguez LJ, Galioto A, Pineo A, Belvedere M (2010) Oral magnesium supplementation improves vascular function in elderly diabetic patients. Magnesium research: official organ of the International Society for the Development of Research on Magnesium 23: 131-137.
- Barragan-Rodriguez L, Rodriguez-Moran M, Guerrero-Romero F (2008) Efficacy and safety of oral magnesium supplementation in the treatment of depression in the elderly with type 2 diabetes: a randomized, equivalent trial. Magnes Res 21: 218-223.
- Mooren FC, Kruger K, Volker K, Golf SW, Wadepuhl M, et al. (2011) Oral magnesium supplementation reduces insulin resistance in non-diabetic subjects - a double-blind, placebo-controlled, randomized trial. Diabetes Obes Metab 13: 281-284.
- McCarty MF (2005) Magnesium may mediate the favorable impact of whole grains on insulin sensitivity by acting as a mild calcium antagonist. Med Hypotheses 64: 619-627.
- Weickert MO, Mohlig M, Schofl C, Arafat AM, Otto B, et al. (2006) Cereal fiber improves whole-body insulin sensitivity in overweight and obese women. Diabetes Care 29: 775-780.
- Liese AD, Roach AK, Sparks KC, Marquart L, D'Agostino RB Jr, et al. (2003) Whole-grain intake and insulin sensitivity: the Insulin Resistance Atherosclerosis Study. Am J Clin Nutr 78: 965-971.
- McKeown NM (2004) Whole grain intake and insulin sensitivity: evidence from observational studies. Nutr Rev 62: 286-291.
- Simental-Mendia LE, Rodriguez-Moran M, Guerrero-Romero F (2014) Oral magnesium supplementation decreases C-reactive protein levels in subjects with prediabetes and hypomagnesemia: a clinical randomized double-blind placebo-controlled trial. Archives of Medical Research 45: 325-330.
Oral magnesium supplementation improves glycaemic status in subjects with prediabetes and hypomagnesaemia: A double-blind placebo-controlled randomized trial
Diabetes & Metabolism, Available online 27 April 2015, doi:10.1016/j.diabet.2015.03.010
F. Guerrero-Romero, L.E. Simental-Mendía, G. Hernández-Ronquillo, M. Rodriguez-Morán rodriguez.moran.martha at gmail.com
This study evaluated the efficacy of oral magnesium supplementation in the reduction of plasma glucose levels in adults with prediabetes and hypomagnesaemia.
A total of 116 men and non-pregnant women, aged 30 to 65 years with hypomagnesaemia and newly diagnosed with prediabetes, were enrolled into a randomized double-blind placebo-controlled trial to receive either 30 mL of MgCl2 5% solution (equivalent to 382 mg of magnesium) or an inert placebo solution once daily for four months. The primary trial endpoint was the efficacy of magnesium supplementation in reducing plasma glucose levels.
At baseline, there were no significant statistical differences in terms of anthropometric and biochemical variables between individuals in the supplement and placebo groups. At the end of follow-up,
- fasting (86.9 ± 7.9 and 98.3 ± 4.6 mg/dL, respectively; P = 0.004) and
- post-load glucose (124.7 ± 33.4 and 136.7 ± 23.9 mg/dL, respectively; P = 0.03) levels,
- HOMA-IR indices (2.85 ± 1.0 and 4.1 ± 2.7, respectively; P = 0.04) and
- triglycerides (166.4 ± 90.6 and 227.0 ± 89.7, respectively; P = 0.009)
were significantly decreased, whereas HDL cholesterol (45.6 ± 10.9 and 46.8 ± 9.2 mg/dL, respectively; P = 0.04) and serum magnesium (1.96 ± 0.27 and 1.60 ± 0.26 mg/dL, respectively; P = 0.005) levels were significantly increased in those taking MgCl2 compared with the controls.
A total of 34 (29.4%) people improved their glucose status (50.8% and 7.0% in the magnesium and placebo groups, respectively; P < 0.0005).
Our results show that magnesium supplementation reduces plasma glucose levels, and improves the glycaemic status of adults with prediabetes and hypomagnesaemia.Type II Diabetes might be prevented and treated with Magnesium – Review Feb 2015
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