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

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Epidemiological evidence suggests that magnesium deficiency may be a factor in the etiology of cardiovascular disease. In the present study, magnesium status was assessed in rabbits 10 weeks following the administration of a diabetogenic dose of alloxan which resulted in significant hyperglycemia and hypoinsulinemia. Decreased erythrocyte magnesium levels were apparent after 6-8 weeks, although no corresponding changes in the magnesium concentration of plasma were apparent. Depletion of magnesium was also observed in left ventricle, spleen, lung, pancreas and aorta. Insulin treatment (for 4 weeks) after 6 weeks of diabetes, prevented the magnesium depletion in both the tissues and red blood cells. Our results provide evidence for alterations in magnesium handling in an experimental model of chronic diabetes.
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PMID:The status of magnesium in rabbits with experimentally-induced diabetes mellitus. 353 35

We assessed the magnesium status in 67 children with insulin-dependent diabetes mellitus (IDDM) in various degrees of diabetic control and its changes during the evolution of the disease. This was done by measuring fasting serum magnesium and 24-hr urinary magnesium clearances when patients were first studied, as well as subsequently on follow-up. In 23 of these patients the retention of intramuscular magnesium was also assessed in relation to the degree of diabetic control and the duration of the illness. The mean +/- SD serum magnesium levels were significantly lower in diabetic children as compared to nondiabetic controls (1.91 +/- 0.22 vs 2.12 +/- 0.26 mg/dl, p less than 0.001). Serum magnesium in diabetic children correlated with glycosylated hemoglobins (r = -0.358, p less than 0.001), but not with 24-hr glycosuria (r = -0.296). On follow-up of patients, serum magnesium significantly increased when IDDM control improved and decreased when the control worsened. Diabetic patients had increased urinary magnesium clearances compared to nondiabetic subjects (5.26 +/- 3.58 vs 3.60 +/- 1.36 cc/min, p less than 0.05). All but five of the 23 patients given the magnesium load retained more than 40% of the dose, with a mean +/- SD retention of 58.7 +/- 5.1%. There was no correlation between the amount of retained magnesium and the duration of the illness, degree of diabetic control, amount of glycosuria, magnesuria, magnesemia, glycosylated hemoglobins, or serum lipids. The data confirm that lower than control serum magnesium levels occur frequently among children with poorly controlled IDDM. Moreover, there might be magnesium deficiency in IDDM, as indicated by the high retention of magnesium when given intramuscularly. The deficiency of this ion may or may not be accompanied by decreased serum magnesium levels and may result from increased urinary magnesium losses in children with IDDM.
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PMID:Magnesium status in children with insulin-dependent diabetes mellitus. 370 Aug 84

In studies concerning risk factors for cardiovascular diseases, a number of reports have emphasized the influence of lipids, but the role of dietary minerals other than sodium has been less studied. However, epidemiological studies have suggested that dietary intake of magnesium and potassium may be involved in such pathogenesis. Studies of the influence of magnesium deficiency on arteriosclerosis include its effect on the initial lesion, altered metabolism of elastin, proliferation of collagen, calcification, lipid metabolism, platelet aggregation and hypertension. Magnesium and potassium metabolism are closely related and magnesium is required for maintaining the level of cellular potassium. As a consequence, magnesium and potassium deficiency frequently occur together and potassium deficiency may be an aggravating factor in pathogenesis. The development of the initial lesion in the arterial wall may be facilitated by loss of cellular magnesium and potassium. Experimental magnesium deficiency induces arterial damage, a loss of magnesium and potassium and an increase in the calcium and sodium content of the cell. Experimental models that have been used to produce cardiovascular lesions induce similar changes and losses of major intracellular cations may affect the main metabolic processes of the cell. This report summarizes the experimental evidence that magnesium deficiency may affect several different stages involved in arteriosclerosis and that potassium deficiency may exacerbate this. Magnesium deficiency results in vascular calcification. Experiments indicate that elastin is the site of the initial calcification and the metabolism of elastin is altered. This vascular lesion then brings about an increase in the collagen content of the wall. Low magnesium status could probably affect this process by slowing collagen resorption and lead to an irreversible accumulation of connective tissue. Results showing a different distribution of the various types of lipoprotein during experimental magnesium deficiency strongly suggest that lipid exchange between the vessel walls and blood can be modified. Severe magnesium deficiency in weanling rats produces a marked hypertriglyceridemia, a decrease in the percentage of cholesterol transported by HDL lipoprotein and a reduction in LCAT activity. The decreased clearance of circulatory triglycerides appears to be the major mechanism contributing to hyperlipemia. Magnesium deficiency could therefore contribute to accumulation of vascular lipid. Magnesium and potassium depletion have also been reported in diabetes and the vascular implications of this should be considered.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of magnesium and potassium in the pathogenesis of arteriosclerosis. 639 44

Diabetes mellitus is the most common pathological state in which secondary magnesium deficiency occurs. Magnesium metabolism abnormalities vary according to the multiple clinical forms of diabetes: plasma magnesium is more often decreased than red blood cell magnesium. Plasma Mg levels are correlated mainly with the severity of the diabetic state, glucose disposal and endogenous insulin secretion. Various mechanisms are involved in the induction of Mg depletion in diabetes mellitus, i.e. insulin and epinephrine secretion, modifications of the vitamin D metabolism, decrease of blood P, vitamin B6 and taurine levels, increase of vitamin B5, C and glutathione turnover, treatment with high levels of insulin and biguanides. K depletion in diabetes mellitus is well known. Some of its mechanisms are concomitant to those of Mg depletion. But their hierarchic importance is not the same: i.e., insulin hyposecretion is more important versus K+ than versus Mg2+. Insulin increases the cellular inflow of K+ more than that of Mg2+ because there is more free K+ (87%) than Mg2+ (30%) in the cell. The consequences of the double Mg-K depletion are either antagonistic: i.e. versus insulin secretion (increased by K+, decreased by Mg2+) or agonistic i.e. on the membrane: (i.e. Na+K+ATPase), tolerance of glucose oral load, renal disturbances. The real importance of these disorders in the diabetic condition is still poorly understood. Retinopathy and microangiopathy are correlated with the drop of plasma and red blood cell Mg. K deficiency increases the noxious cardiorenal effects of Mg deficiency. The treatment should primarily insure diabetic control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Magnesium and potassium in diabetes and carbohydrate metabolism. Review of the present status and recent results. 639 45

There is accumulating evidence that the metabolism of several trace elements is altered in insulin-dependent diabetes mellitus and that these nutrients might have specific roles in the pathogenesis and progress of this disease. Magnesium deficiency is the most evident disturbance of metal metabolism in diabetes mellitus. Hypomagnesemia might increase the risk of ischemic heart disease and severe retinopathy. Increased urinary loss of zinc is a commonly encountered feature of diabetes. High-dose oral zinc might enhance wound healing, although data regarding diabetes are lacking. Chromium increases tissue sensitivity to insulin and tends to raise high-density lipoprotein (HDL) cholesterol and the HDL:low-density lipoprotein ratio. Selenium is involved in processes which protect the cell against oxidative damage by peroxides produced from lipid metabolism. There is one report of elevated serum selenium in diabetic children although the clinical significance of this finding is still unclear. An insulin-like effect has recently been attributed to vanadium in experimental animals, a finding of potential interest to man. Current knowledge does not implicate iron, iodine, manganese, cobalt, nickel, silicone, fluoride, molybdenum or tin in the pathophysiology of diabetes. Appropriate trace element supplementation might prove beneficial in ameliorating some physiological deficiencies associated with diabetes and prevent or retard secondary complications. However, properly designed and well-documented trials, especially on magnesium supplementation, need to be performed before rationales for such supplementation are developed. The potential roles of vanadium, chromium and selenium in diabetes constitute challenging areas for further experimental and clinical research.
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PMID:The role of trace elements in juvenile diabetes mellitus. 640 Apr 52

Magnesium deficiency and its association with platelet hyperreactivity has been well recognised in a variety of diseases including myocardial infarction, preeclampsia, and diabetes. In order to investigate potential effects of intravenous Mg2+ supplementation, platelet function was studied by measurements of in vitro bleeding time (BT) and of fibrinogen (Fg)-mediated aggregation of washed platelets. In addition, the effect of Mg2+ on platelet adhesion onto immobilised Fg, on Fg binding to activated platelets, and on surface expression of GMP-140 or GP53 was evaluated. Mg2+ (4 mM) prolonged in vitro BT by 30% and inhibited Fg-mediated aggregation significantly, independent of the agonist used to initiate platelet aggregation (ADP, collagen, epinephrine, thrombin, phorbol ester). Adhesion of resting platelets to immobilised Fg was reduced by 50% in the presence of 2 mM Mg2+. Moreover, Mg2+ reduced Fg binding to ADP- or collagen-stimulated platelets as well as surface expression of GMP-140 with an IC50 of approximately 3 mM. Intravenous administration of Mg2+ to healthy volunteers inhibited both ADP-induced platelet aggregation (p < 0.05) by 40% and binding of Fg or surface expression of GMP-140 by 30% (p < 0.05). Thus, pharmacological concentrations of Mg2+ effectively inhibit platelet function in vitro and ex vivo.
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PMID:Effects of magnesium on platelet aggregation and adhesion. Magnesium modulates surface expression of glycoproteins on platelets in vitro and ex vivo. 774 Apr 63

In newly diagnosed insulin-dependent diabetes mellitus, the mechanisms underlying the concomitant occurrence of magnesium deficiency and normal blood magnesium concentration are unknown. The renal handling of magnesium was, therefore, studied in 37 children with newly diagnosed insulin-dependent diabetes mellitus and in 13 controls. Circulating magnesium levels were similar in patients and controls (0.86 vs. 0.84 mmol/l). However, the urinary excretion of magnesium was significantly higher in patients (90.6 vs. 32.2 mumol/l GFR). In the patients a significant positive correlation was found between excretion of magnesium and glycosuria or blood hydrogen ion activity. It is concluded that osmotic diuresis and acidosis increase magnesium excretion in newly diagnosed diabetes mellitus.
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PMID:Hypermagnesiuria in children with newly diagnosed insulin-dependent diabetes mellitus. 797 81

The interrelationships between magnesium and carbohydrate metabolism have regained considerable interest over the last few years. Insulin secretion requires magnesium: magnesium deficiency results in impaired insulin secretion while magnesium replacement restores insulin secretion. Furthermore, experimental magnesium deficiency reduces the tissues sensitivity to insulin. Subclinical magnesium deficiency is common in diabetes. It results from both insufficient magnesium intakes and increase magnesium losses, particularly in the urine. In type 2, or non-insulin-dependent, diabetes mellitus, magnesium deficiency seems to be associated with insulin resistance. Furthermore, it may participate in the pathogenesis of diabetes complications and may contribute to the increased risk of sudden death associated with diabetes. Some studies suggest that magnesium deficiency may play a role in spontaneous abortion of diabetic women, in fetal malformations and in the pathogenesis of neonatal hypocalcemia of the infants of diabetic mothers. Administration of magnesium salts to patients with type 2 diabetes tend to reduce insulin resistance. Long-term studies are needed before recommending systematic magnesium supplementation to type 2 diabetic patients with subclinical magnesium deficiency.
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PMID:[Magnesium and glucose metabolism]. 809 58

Magnesium status may be compromised with ageing for two reasons: insufficient intake (magnesium deficiency) or alterations in magnesium metabolism (magnesium depletion). There is a large volume of literature suggesting that magnesium deficit contributes to the ageing process and to the vulnerability to age-related diseases. One of the biological changes associated with ageing is an increase in free radical formation with subsequent damage to cellular processes. Prime targets of the more reactive free radicals are unsaturated lipids in cell membranes, amino acids in proteins, and nucleotides in DNA. The accumulation of unrepaired oxidative damage products may be a major factor in cellular ageing. Magnesium-deficient animals show an increased susceptibility to an in vivo oxidative stress and their tissues are more susceptible to in vitro peroxidation. Moreover, the protective properties of various antioxidant drugs and nutrients suggest that free radicals are involved in the injury process of magnesium deficiency. The consequences on stress susceptibility, defective membrane functions and perturbation of intracellular calcium metabolism, inflammation, cardiovascular diseases including atherosclerosis and ischaemia/reoxygenation injury, diabetes, fibrosis, immune dysfunction and other diseases associated with ageing are presented and discussed.
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PMID:Magnesium and ageing. I. Experimental data: importance of oxidative damage. 815 89


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