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The aim of this paper is to discuss, on the basis of an extensive literature review, the role of magnesium in health and disease. Magnesium is an essential cation playing a crucial role in many physiological functions. It is critical in energy-requiring metabolic processes, in protein synthesis, membrane integrity, nervous tissue conduction, neuromuscular excitability, muscle contraction, hormone secretion, and in intermediary metabolism. Serum magnesium concentration is maintained within a narrow range by the small intestine and kidney which both increase their fractional magnesium absorption under conditions of magnesium deprivation. If magnesium depletion continues, the bone store helps to maintain serum magnesium concentration by exchanging part of its content with extracellular fluid. The abundance of magnesium within cells is consistent with its relevant role in regulating tissue and cell functions. Recent data suggest that large fluxes of magnesium can cross the cell plasma membrane in either direction following a variety of hormonal and non-hormonal stimuli, resulting in major changes in total and, to a lesser extent, in free magnesium content within tissues. Imbalances of magnesium are common and are associated with a great number of pathological situations responsible for human morbidity and mortality. A large part of the population may have an inadequate magnesium intake, and in particular elderly subjects and athletes may be prone to chronic latent magnesium deficiency. Magnesium deficit is frequently observed in alcoholics and diabetic patients, in whom a combination of factors contributes to its pathogenesis. We will discuss some of the aspects of the involvement of magnesium in the etiology of some pathological situations, such as cardiovascular diseases, diabetes, pre-eclampsia, eclampsia, sickle cell disease and chronic alcoholism.
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PMID:Role of cellular magnesium in health and human disease. 1476 64

A tendency for magnesium deficiency in patients with diabetes mellitus is well established, which probably results from glycosuria-related hypermagnesiuria, nutritional factors or hyperinsulinaemia. Hypomagnesaemia is probably a secondary event but it can also lead to insulin resistance itself. The offspring of patients with Type 2 diabetes mellitus (T2DM) are at increased risk of developing diabetes and several metabolic abnormalities of the disease. The aim of this study was to determine if serum total magnesium levels in healthy offspring of T2DM patients underwent alterations and their relationship to indicators of glucose homeostasis. The sample consisted of two groups: 30 healthy offspring with at least one diabetic parent, and 30 age-matched healthy subjects with no family history of T2DM. None of the participants was on a diet. The mean serum magnesium concentration was 1.070 +/- 0.059 mmol/l in offspring and 1.075 +/- 0.084 mmol/l in controls (p=0.66). There was no statistically significant correlation between serum magnesium levels and parameters of glucose homeostasis in offspring. Our results support the conclusion that total serum magnesium probably has no relationship with the main indicators of glucose homeostasis in offspring of T2DM patients and is not likely to be a fundamental risk factor for the development of insulin resistance.
Diabetes Nutr Metab 2004 Feb
PMID:Serum magnesium levels in non-diabetic offspring of patients with Type 2 diabetes mellitus. 1516 19

Recent epidemiology has linked high consumption of whole grains with reduced risk for diabetes, coronary disease, stroke, and various types of cancer; there is reason to suspect that improved insulin sensitivity is largely responsible for this protection. This phenomenon may be partially explained by the lower glycemic indices of some whole grain food products in comparison to their fiber-depleted analogs. Nonetheless, the fact that whole wheat flour promotes insulin sensitivity relative to white flour--and yet has a near-identical glycemic index--suggests that certain nutrients or phytochemicals in whole wheat, depleted by the refining process, promote preservation of insulin sensitivity. Magnesium is a likely candidate in this regard; magnesium deficiency promotes insulin resistance in rodents and in humans, whereas supplemental magnesium has been found to prevent type 2 diabetes in rodent models of this syndrome, and to improve the insulin sensitivity of elderly or diabetic humans. Magnesium-rich diets as well as above-average serum magnesium are associated with reduced diabetes risk in prospective epidemiology, and with greater insulin sensitivity in cross-sectional studies; moreover, other types of magnesium-rich foods--dairy products, legumes, and nuts--have been linked to decreased diabetes risk in prospective studies. The biochemical role of magnesium in support of insulin function is still poorly understood. In light of evidence that magnesium can function as a mild natural calcium antagonist, it is interesting to note suggestive evidence that increases in intracellular free calcium may compromise the insulin responsiveness of adipocytes and skeletal muscle, and may indeed play a pathogenic role in the insulin resistance syndrome. Thus, it is proposed that some or all of the favorable impact of good magnesium status on insulin function may reflect antagonism of the induction or effects of increased intracellular free calcium. Further research concerning the potential health benefits of long-term magnesium supplementation is clearly warranted. These considerations, however, should not detract from efforts to better inform the public regarding the strong desirability of choosing whole grain products in preference to refined grains.
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PMID:Magnesium may mediate the favorable impact of whole grains on insulin sensitivity by acting as a mild calcium antagonist. 1561 78

Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of diabetes complications. Previous studies have shown that magnesium decreases basal tone in normal isolated aortic rings and reduces phenylephrine-induced contraction. The mechanism of this magnesium action is not very well known. The present study was designed to determine the role of endothelium and nitric oxide in magnesium sulfate-induced vasorelaxation in diabetic rat vessels. Diabetes was induced by a single tail injection of streptozotocin. Eight weeks later, superior mesenteric arteries of control and diabetic animals were isolated and perfused according to the McGregor method. Prepared vascular beds were constricted with phenylephrine to induce 70-75% of maximal constriction. Magnesium sulfate at concentrations of 0.001 M to 0.1 M was added into the medium and perfusion pressure was then recorded. Mesenteric bed baseline perfusion pressure in intact and denuded endothelium of diabetic groups was higher than controls. In all groups, relaxant response to magnesium in mesenteric bed was attenuated after endothelium removal, but a relaxatory effect appears at high concentration. In the presence of N (omega)-nitro-L-arginine methyl ester (L-NAME), magnesium-induced relaxation was significantly suppressed in intact mesenteric bed of control animals but in diabetics, the relaxant response was slightly inhibited. From the results of this study, it can be concluded that magnesium-induced endothelium dependent and endothelium independent vasorelaxation are mediated by nitric oxide in control rats while in diabetic animals other mechanisms may be involved.
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PMID:Relaxatory effect of magnesium on mesenteric vascular beds differs from normal and streptozotocin induced diabetic rats. 1568 Feb 69

Vascular disease is one of the complicating features of diabetes mellitus. Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of diabetes complications. Several studies have indicated that hypertension in diabetic patients is an independent altered reaction of blood vessels to neurotransmitters and circulating hormones. Since magnesium has been proposed to decrease vascular sensitivity to vasoconstrictor agents, the present study was designed to determine whether chronic magnesium sulfate administration could prevent vascular complications of STZ-induced diabetes in rats. The animals were divided into six groups: two groups served as controls and received tap water for 8 weeks, while in the other four groups, made diabetic with a single IV injection of 40 mg/kg STZ, two groups treated with magnesium sulfate (10 g/L) added to the drinking water, and the other two groups received tap water only. After 8 weeks, in 3 groups (control, diabetic and Mg-treated), left common carotid artery was cannulated for continuous recording of blood pressure. All animals in these groups were decapitated and blood samples were drawn for glucose, Ca and Mg measurements. In the 3 remaining groups (again divided into control, diabetic and Mg-treated), the mesenteric vascular bed was perfused according to the McGregor method, and descending thoracic aortas were used for measurement of elasticity. In diabetic rats, plasma glucose was significantly increased and plasma magnesium was significantly decreased compared to controls and Mg-treated animals. Although plasma magnesium of Mg-treated animals increased significantly, it failed to reach to the magnesium level of the control group. Ca/Mg ratio was also increased compared to the control and Mg-treated animals. Mean arterial blood pressure in diabetics was significantly higher than control and Mg-treated rats. Similarly, there was a significant difference in mean arterial blood pressure of Mg-treated rats compared to control animals. Baseline perfusion pressure of diabetic group was significantly higher than control and Mg-treated groups with intact and denuded endothelium. Magnesium sulfate treatment decreased mean perfusion pressure of mesenteric vascular bed in intact and denuded endothelium in comparison with non-treated diabetic rats. There was a significant increase in passive tension in the aorta of diabetic rats compared to control and Mg-treated rats. However, there was no significant difference between Mg-treated and control rats. From the results of this study it may be concluded that magnesium could control STZ-induced diabetes and prevent its vascular complications.
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PMID:Oral magnesium administration prevents vascular complications in STZ-diabetic rats. 1568 Mar 10

Electrolyte balance is a critical issue in managing comorbid conditions in both diseased and elderly patients. Patients with hypertension and diabetes need careful regulation of their calcium and magnesium levels, whereas in patients with congestive heart failure, sodium and potassium levels also are critical. Herein we report the outcome of a round table discussion at which issues of renal magnesium clearance, magnesium and arrhythmic risk, ion balance in heart failure, diabetes, ischemic stress, oxidative stress in the cardiomyopathy of magnesium deficiency, roles of magnesium and potassium in bone metabolism and the aging population, and the role of electrolyte balance in hypertension have been discussed. In all these issues the maintaining homeostasis of potassium and magnesium is critical and the various therapies that impact on retaining these ions were discussed. Hallmark studies, i.e., Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial and Studies of Left Ventricular Dysfunction, have provided insight into treatment of patients with cardiovascular and progressive heart failure. These studies and the availability of potassium- and magnesium-sparing diuretics for use in these disorders provide relevant perspectives for treatment.
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PMID:Potassium, magnesium, and electrolyte imbalance and complications in disease management. 1577 33

1. Magnesium deficiency has recently been proposed as a novel factor implicated in the pathogenesis of the complications of diabetes. The purpose of the present study was to determine the relationship between oral Mg supplementation and changes in plasma glucose, calcium, haemoglobin, Ca/Mg ratio, blood pressure and the histology of the pancreas and vascular system in streptozotocin-induced diabetic rats. 2. Ten days after the induction of diabetes in male Wistar rats, half the diabetic animals were divided into six groups, receiving 0, 1, 3, 10, 30 or 50 g/L MgSO4 added into the drinking water for 8 weeks. Plasma glucose and Mg were measured at days 1, 2, 3, 5, 7, 14 and 21 to find the optimum dose of Mg and the time-course of its effect. In addition, histological observations were undertaken. Eight weeks later, all animals were decapitated, the pancreas and thoracic aorta were removed carefully and immersed immediately in 10% formaldehyde for histological study. 3. To evaluate the effects of Mg on plasma glucose, calcium, haemoglobin, Mg and blood pressure, another group of animals was divided into four experimental groups, as follows: (i) non-diabetic controls received tap water for 8 weeks; (ii) acute diabetics received tap water for 10 days; (iii) chronic diabetic controls received tap water for 8 weeks; and (iv) Mg-treated chronic diabetic rats received 10 g/L MgSO4 added into the drinking water 10 days after the induction of diabetes for 8 weeks. 4. Magnesium dose dependently affects plasma glucose levels. The peak effect was reached during the first 24 h following oral administration. Administration of 10 g/L MgSO4 results in the return of normal structure in the diabetic pancreas and aorta. Moreover, this concentration of MgSO4 causes glucose, haemoglobin, calcium, the Ca/Mg ratio and blood pressure to reach normal levels. Although the Mg level increases slightly following the administration of 10 g/L MgSO4 to diabetic rats, it never reaches control levels. 5. On the basis of the results of the present study, it may be concluded that chronic Mg administration may have beneficial effects on diabetes.
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PMID:Effects of administration of oral magnesium on plasma glucose and pathological changes in the aorta and pancreas of diabetic rats. 1612 Jan 85

The average dietary intake of magnesium is below recommended dietary allowances in many affluent Western countries. Prolonged low magnesium intake tends to result in hypomagnesaemia which might increase the risk of chronic diseases in elderly people. A national population-based cross-sectional nutrition survey, the Elderly Nutrition and Health Survey in Taiwan (1999-2000), was used to investigate the magnesium status and association with diabetes in the Taiwanese elderly. Dietary magnesium intake was based on 24-hour dietary recalls. Blood biochemical parameters including plasma magnesium and blood glucose were also measured. Average magnesium intake was 250 mg in men and 216 mg in women, which is equivalent to 68-70% of relevant Taiwanese Dietary Reference Intakes. The mean plasma magnesium concentration was 0.903 mmol/L in men and 0.906 mmol/L in women. The prevalence of a plasma magnesium level of <0.7 mmol/L was 0.7-0.9% in the elderly, and that of <0.8 mmol/L was 8.0-9.1%. Elderly vegans had a significantly lower magnesium intake than ovo-lacto vegetarians and non-vegetarians. Diabetic men and women had significantly higher blood glucose levels than non-diabetics. The risk of diabetes was elevated 3.25 times at plasma magnesium levels<0.863 mmol/L. There was an inverse association between plasma magnesium concentration and the prevalence of diabetes. However, no association was found between diabetes and low dietary magnesium. Taiwanese elderly persons had suboptimal levels of dietary magnesium intake, which although may be sufficient to avoid overt magnesium deficiency, may not be sufficient to reduce the risk of diabetes in the elderly. Further prospective study is required to help explain the differential results between dietary and plasma magnesium levels.
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PMID:Magnesium status and association with diabetes in the Taiwanese elderly. 1616 38

Magnesium is a predominantly intracellular ion, and it is a cofactor in more than 300 enzymatic reactions, like tyrosinokinase activity. Its deficiency may increase insulin resistance, especially in patients with metabolic syndrome or type 2 diabetes. This study evaluated in 27 patients with poorly controlled type 2 diabetes if there was correlation between intracellular magnesium levels, laboratorial indexes of insulin resistance and glycemic control. Decreased serum and intracellular magnesium depletion were found in 75% and 30.8% of patients, respectively. A negative correlation between intracellular magnesium levels (ICMg) and BMI and HbA1 was found. The homeostasis model assessment for insulin resistance (HOMA-IR) was higher than 3.0 in 59.2% of patients and there was a tendency to negative correlation with ICMg levels, although without statistical significance. Despite the small number of patients, this study shows that magnesium deficiency is frequent in patients with diabetes and its correlation with insulin resistance should be more studied.
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PMID:[Magnesium deficiency and insulin resistance in patients with type 2 diabetes mellitus]. 1654 20

The aim of this review was to elaborate a synthesis about the discussions on magnesium and diabetes mellitus, in the last 14 years. The magnesium deficiency has been associated with chronic diseases, amongst them, diabetes mellitus. Epidemiological studies had shown low levels of magnesium ingestion in the general population, as well as a relation between the ingestion of food rich in magnesium and the reduction of diabetes installation and its complications. Hypomagnesemia is frequently present in diabetic patients, however there is not an exact elucidation of the mechanism of magnesium deficiency in diabetes mellitus. On the other hand, in the presence of this illness, it is observed that inadequate metabolic control can affect the corporal concentrations of magnesium, developing hypomagnesemia, which may be still directly related with some micro and macrovascular complications observed in diabetes, as cardiovascular disease, retinopathy and neuropathy. This way, the chronic complications of diabetes can appear precociously. Based on this, the supplementation with magnesium has been suggested in patients with diabetes mellitus who have proven hypomagnesemia and the presence of its complications.
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PMID:Magnesium and diabetes mellitus: their relation. 1669 Jan 76


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