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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is unclear whether insulin-dependent diabetes mellitus is a state of magnesium depletion. This is a relevant question, since magnesium deficiency has been implicated in the pathogenesis of diseases that develop to an increased extent into diabetes mellitus. Total plasma magnesium was not statistically different in 76 pediatric patients with insulin-dependent diabetes mellitus (0.77 [0.73-0.81] mmol/l; median and interquartile range), 59 healthy adults (0.80 [0.77-0.83] mmol/l) and 19 healthy children (0.80 [0.78-0.83] mmol/l). In contrast, plasma ionized magnesium, the most interesting form with respect to physiological and biological properties, was significantly lower in diabetic patients (0.50 [0.48-0.53] mmol/l) when compared with healthy adults (0.53 [0.50-0.56] mmol/l; p < 0.01) and healthy children (0.54 [0.51-0.56] mmol/l; p < 0.02). Our report confirms recent findings of reduced circulating ionized magnesium but normal circulating total magnesium in adults with non-insulin-dependent diabetes mellitus.
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PMID:Extracellular magnesium depletion in pediatric patients with insulin-dependent diabetes mellitus. 925 79

A tendency for magnesium deficiency in patients with diabetes mellitus is well-established. Glucosuria-related hypermagnesiuria, nutritional factors and hyperinsulinaemia-related hypermagnesiuria all can contribute. The plasma magnesium level has been shown to be inversely related to insulin sensitivity. Magnesium supplementation improves insulin sensitivity as well as insulin secretion in patients with type 2 diabetes. Nevertheless, no beneficial effects of oral magnesium supplementation has been demonstrated on glycaemic control either in patients with diabetes type 1 or 2. Oral magnesium supplementation reduced the development of type 2 diabetes in predisposed rats. There are some indications that magnesium decreases blood pressure, but negative results have been observed in trials that were, however, not designed to test effect on blood pressure as primary parameter. Patients with (severe) retinopathy have a lower plasma magnesium level compared to patients without retinopathy and a prospective study has shown the plasma magnesium level to be inversely related to occurrence or progression of retinopathy. Further study on magnesium (supplementation) is warranted in the prevention of type 2 and of (progression of) retinopathy as well as a means to reduce high blood pressure.
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PMID:Magnesium in diabetes mellitus. 1021 82

Vitamin E is an antioxidant that has been demonstrated to improve insulin action. Glutathione, another natural antioxidant, may also be important in blood pressure and glucose homeostasis, consistent with the involvement of free radicals in both essential hypertension and diabetes mellitus. Our group has recently suggested that the effects of reduced glutathione on glucose metabolism may be mediated, at least in part, by intracellular magnesium levels (Mg([i])). Recent evidence suggests that vitamin E enhances glutathione levels and may play a protective role in magnesium deficiency-induced cardiac lesions. To directly investigate the effects of vitamin E supplementation on insulin sensitivity in hypertension, in relation to the effects on circulating levels of reduced (GSH) and oxidized (GSSG) glutathione and on Mg([i]), we performed a 4-week, double-blind, randomized study of vitamin E administration (600 mg/d) versus placebo in 24 hypertensive patients and measured whole-body glucose disposal (WBGD) by euglycemic glucose clamp, GSH/GSSG ratios, and Mg([i]) before and after intervention. The relationships among WBGD, GSH/GSSG, and Mg([i]) in both groups were evaluated. In hypertensive subjects, vitamin E administration significantly increased WBGD (25.56+/-0.61 to 31.75+/-0.53 micromol/kg of fat-free mass per minute; P<0.01), GSH/GSSG ratio (1.10+/-0.07 to 1.65+/-0.11; P<0.01), and Mg([i]) (1.71+/-0.042 to 1.99+/-0.049 mmol/L; P<0.01). In basal conditions, WBGD was significantly related to both GSH/GSSG ratios (r=0.58, P=0.047) and Mg([i]) (r=0.78, P=0.003). These data show a clinical link between vitamin E administration, cellular magnesium, GSH/GSSG ratio, and tissue glucose metabolism. Further studies are needed to explore the cellular mechanism(s) of this association.
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PMID:Effects of vitamin E and glutathione on glucose metabolism: role of magnesium. 1052 98

This review deals with the six main clinical situations related to magnesium or one of its fractions, including ionized magnesium: renal disease, hypertension, pre-eclampsia, diabetes mellitus, cardiac disease, and the administration of therapeutic drugs. Issues addressed are the physiological role of magnesium, eventual changes in its levels, and how these best can be monitored. In renal disease mostly moderate hypermagnesemia is seen; measuring ionized magnesium offers minimal advantage. In hypertension magnesium might be lowered but its measurement does not seem relevant. In the prediction of severe pre-eclampsia, elevated ionized magnesium concentration may play a role, but no unequivocal picture emerges. Low magnesium in blood may be cause for, or consequence of, diabetes mellitus. No special fraction clearly indicates magnesium deficiency leading to insulin resistance. Cardiac diseases are related to diminished magnesium levels. During myocardial infarction, serum magnesium drops. Total magnesium concentration in cardiac cells can be predicted from levels in sublingual or skeletal muscle cells. Most therapeutic drugs (diuretics, chemotherapeutics, immunosuppressive agents, antibiotics) cause hypomagnesemia due to increased urinary loss. It is concluded that most of the clinical situations studied show hypomagnesemia due to renal loss, with exception of renal disease. Keeping in mind that only 1% of the total body magnesium pool is extracellular, no simple measurement of the real intracellular situation has emerged; measuring ionized magnesium in serum has little added value at present.
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PMID:Magnesium in disease: a review with special emphasis on the serum ionized magnesium. 1072 9

There is an increased interest in the role of magnesium ions in clinical medicine, nutrition and physiology. The characteristics of the binding of magnesium and calcium ions to various components, macromolecules and biological membranes are described. Magnesium affects many cellular functions, including transport of potassium and calcium ions, and modulates signal transduction, energy metabolism and cell proliferation. The mechanism of cellular uptake and efflux of magnesium, its intracellular transport, intestinal absorption, renal excretion and the effect of hormones on these are reviewed. Magnesium deficiency is not uncommon among the general population: its intake has decreased over the years especially in the western world. The magnesium supplementation or intravenous infusion may be beneficial in various diseased states. Of special interest is the magnesium status in alcoholism, eclampsia, hypertension, atherosclerosis, cardiac diseases, diabetes, and asthma. The development of instrumentation for the assay of ionized magnesium is reviewed, as are the analytical procedures for total magnesium in blood and free magnesium in the cytosol. The improved procedures for the assay of different magnesium states are useful in understanding the role of magnesium in health and disease.
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PMID:Magnesium. An update on physiological, clinical and analytical aspects. 1072 69

Magnesium deficiency is a common clinical condition that may exist despite a normal serum magnesium concentration. Patients with chronic pancreatitis could develop magnesium deficiency due to either malabsorption, diabetes mellitus, or chronic alcoholism. Since serum levels of magnesium are a poor indicator of magnesium deficiency, the retention of a low-dose intravenous magnesium load (0.1 mmol/kg body weight) was determined in 13 patients with chronic pancreatitis (10 due to alcoholism) and eight healthy controls. Percentage magnesium retention was greater in patients with chronic pancreatitis than controls (59.8+/-37.3% S.D. versus 22.0+/-38.2% S. D.: P=0.038), and 10 of 13 patients showed evidence of magnesium deficiency. Routine evaluation of magnesium status could allow appropriate supplementation and conceivably symptomatic improvement in patients with severe chronic pancreatitis.
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PMID:Magnesium deficiency in patients with chronic pancreatitis identified by an intravenous loading test. 1107 71

Magnesium is the fourth most abundant cation in the body and is present in more than 300 enzymatic systems, where it is crucial for adenosine triphosphate (ATP) metabolism. Deficiency states result in increased insulin resistance, as well as increased smooth muscle and platelet reactivity. Magnesium deficiency has been shown to correlate with a number of chronic cardiovascular diseases, including hypertension, diabetes mellitus, and hyperlipidemia. Intravenous magnesium has been used therapeutically in critical situations such as status asthmaticus, torsades de pointes, and preeclampsia. Few controlled studies exist regarding the therapeutic uses of oral magnesium supplementation in chronic cardiovascular diseases. Randomized clinical trials are urgently needed to determine whether magnesium supplementation will alter the natural history of these disease states.
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PMID:Magnesium: its proven and potential clinical significance. 1260 35

Magnesium deficit and oxidative stress are common features of the diabetic state. This concept supported by another observation that magnesium deficiency is also a state of increased oxidative stress prompted us to study the effect of magnesium supplementation on magnesium status and oxidative stress in diabetic rats. For this purpose, male Wistar rats were made diabetic with a single intraperitoneal injection of Alloxan. Experimental diabetes caused a significant decrease in serum and red blood cell magnesium levels and increased urinary excretion of magnesium. Marked increase in plasma malondialdehyde and corresponding decrease in vitamins C & E, uric acid and total thiols was observed in the diabetic rats as compared to control group. In liver, MDA levels were increased significantly with concomitant decrease in vitamin C, non-protein thiols and antioxidant enzymes (SOD & GST). Magnesium supplementation for four weeks restored serum and RBC magnesium levels to near normal levels with marginal but significant decrease in blood glucose levels. Plasma and liver MDA levels were reduced significantly and vitamin C and total thiols were increased significantly with magnesium supplementation. Antioxidant enzyme activity was also increased significantly with magnesium supplementation in diabetic rats. Our data clearly demonstrates that alloxanic diabetes is associated with decreased magnesium status and increased oxidative stress and that magnesium supplementation can in part restore the antioxidant parameters and decrease the oxidative stress in experimental diabetic rats.
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PMID:Effect of magnesium supplementation on oxidative stress in alloxanic diabetic rats. 1273 78

African-Americans are known to be disproportionately impacted by many chronic diseases such as diabetes, hypertension, cardiovascular, and renal disease. Lower levels of dietary and serum magnesium have been associated with an increased prevalence of hypertension, insulin resistance, and diabetes. Studies suggest a greater prevalence of occult magnesium deficiency among African-Americans compared to other populations. This increased prevalence of hypomagnesemia may contribute to increased insulin resistance leading to accelerated atherosclerosis and premature death. Trials that correct magnesium status/levels among African-Americans, whether through dietary intervention or direct magnesium replacement/supplementation need to be completed to characterize this relationship more completely.
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PMID:Magnesium deficiency in African-Americans: does it contribute to increased cardiovascular risk factors? 1274 15

Magnesium plays an essential role in many biochemical and physiological processes. Homeostasis of magnesium is tightly regulated and depends on the balance between intestinal absorption and renal excretion. During the last decades, various hereditary disorders of magnesium handling have been clinically characterized and genetic studies in affected individuals have led to the identification of some molecular components of cellular magnesium transport. In addition to these hereditary forms of magnesium deficiency, recent studies have revealed a high prevalence of latent hypomagnesemia in the general population. This finding is of special interest in view of the association between hypomagnesemia and common chronic diseases such as diabetes, coronary heart disease, hypertension, and asthma. However, valuable methods for the diagnosis of body and tissue magnesium deficiency are still lacking. This review focuses on clinical and genetic aspects of hereditary disorders of magnesium homeostasis. We will review primary defects of epithelial magnesium transport, disorders associated with defects in Ca(2+)/ Mg(2+) sensing, as well as diseases characterized by renal salt wasting and hypokalemic alkalosis, with special emphasis on disturbed magnesium homeostasis.
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PMID:Genetics of hereditary disorders of magnesium homeostasis. 1463 61


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