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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between magnesium levels and oxygen uptake in patients with non-insulin dependent diabetes mellitus (NIDDM) without apparent visceral dysfunction was studied. Magnesium levels in plasma, erythrocytes and urine as well as oxygen uptake parameters were determined in NIDDM patients and controls. Oxygen uptake parameters were measured with an exercise ergometer and expired gas analysis according to Wasserman et al. Low oxygen uptake in NIDDM patients was correlated significantly with plasma and erythrocyte magnesium levels, but not with urinary magnesium excretion. In NIDDM patients, higher correlation coefficients were seen between oxygen uptake parameters at peak in men and at the anaerobic threshold in women and plasma or erythrocyte magnesium levels. These results confirm previous results indicating that plasma and erythrocyte magnesium levels in NIDDM patient are decreased, and further demonstrate that the decreased magnesium levels are positively correlated with oxygen uptake. Although the mechanism remains to be established, it is possible that the magnesium deficiency in NIDDM patients due to environmental or genetic factors may result in low oxygen uptake and decreased work capacity.
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PMID:Plasma and erythrocyte magnesium levels are correlated with oxygen uptake in patients with non-insulin dependent diabetes mellitus. 970 Apr 83

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

Magnesium deficit is associated with several acute and chronic illnesses. Of major concern is the association between cardiovascular problems, such as myocardial infarction, hypertension, congestive heart failure, and hypomagnesemia. In addition, evidence is mounting regarding the relationship between Type II Diabetes Mellitus, and magnesium deficit. The American diet is low in magnesium, and with modern water systems, very little is ingested in the drinking water. A review of the state of the science in relation to literature on magnesium follows, as well as nursing interventions crucial to managing magnesium deficit.
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PMID:Hypomagnesemia in acute and chronic illness. 1185 22

Imbalances between mineral intakes and recommended amounts have been observed in different groups of elderly subjects. Nevertheless, assessment of the status of magnesium and trace elements in the elderly is difficult, even for iron because infection and inflammation increases ferritin. Mineral bioavailability may change due to ageing. Therefore, formulation of mineral recommendations is complex and individual recommendations are sometimes necessary. A number of surveys show magnesium, zinc, selenium and chromium intakes by old persons to be lower than the corresponding reference nutrient intakes. Contrarily, intakes of iron are generally adequate or higher than recommended, and it has been suggested that increased storage of iron in the elderly may be related with the development of age-related diseases through the increase in oxidative stress. Low iron status together with iron excess may be common in an elderly population. The same applies for zinc. Magnesium and selenium deficiencies among the elderly are also well documented, especially among the institutionalised and people with pathologies. Chromium deficiency is associated with type II diabetes mellitus. Recommended iron intake is lower for elderly women compared to young, because menstruation ceases after menopause, but in old men, it is similar to that of young men. Dietary Reference Values for the rest of the elements are similar to those of adults, although several suggestions have been made about the quantities. This review examines various aspects of the changes in mineral bioavailability due to ageing, of data published on mineral intakes and status, and finally the dietary recommendations for this vulnerable population group.
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PMID:Magnesium and trace elements in the elderly: intake, status and recommendations. 1216 71

Magnesium (Mg(2+)), the second most abundant intracellular cation, is a critical cofactor in numerous enzymatic reactions. By using a fluorescent probe, mag-fura-2, we examined the basal levels and changes in intracellular Mg(2+)([Mg(2+)](i)) of platelets in diabetic and obese children. Under the basal condition, the platelet [Mg(2+)](i) of both type 1 and type 2 diabetes mellitus (DM) and the obesity groups was significantly lower than the values in the nondiabetic control group (377 +/- 62 micromol/L, 312 +/- 72 micromol/L, 373 +/- 35 micromol/L v 594 +/- 62 micromol/L, respectively, P <.05). [Mg(2+)](i) was increased after the stimulation with 100 microU/mL of insulin. After 60 seconds of insulin stimulation, the value of [Mg(2+)](i) was lower in the type 1 DM group compared with the control group (729 +/- 85 micromol/L v 1,078 +/- 67 micromol/L, P <.005). The increase in percentage over the resting [Mg(2+)](i) was higher in the type 2 DM group than in the stimulated control group (222% +/- 51% v 98% +/- 18 %, P <.05), although the stimulated [Mg(2+)](i) did not reach the level of the control group. The diabetic patients and obese subjects have [Mg(2+)](i) deficiency. In the type 2 DM and obese groups, platelets responded well to insulin. In children under insulin-resistant states, [Mg(2+)](i) decreases before the poor reactivity to insulin occurs in platelets. Decreased [Mg(2+)](i) might underlie the initial pathophysiologic events leading to insulin resistance and abnormality of platelet coagulation.
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PMID:Intracellular magnesium of platelets in children with diabetes and obesity. 1270 Oct 60

A previously unknown genetic defect in magnesium metabolism (i.e., the magnesium-binding defect [MgBD]) was found to be associated with the cause of "salt-sensitive" essential hypertension in humans and rats. It inhibits the entrance of Mg2+ into the cell so that the intracellular concentrations of Mg2+ and MgATP2- are decreased. Consequently, the 300 enzyme reactions in the cell, especially the 100 that either use or produce MgATP2-, are inhibited. Thus, because the extrusion of intracellular Na+ requires MgATP2-, hypertension results when the involved MgATP2- requiring enzyme is inhibited. The MgBD is corrected by the tachykinin substance P, which occurs in normal blood plasma, and by the pentapeptide and its contained tetrapeptide, which are released from the C-terminal region of substance P by plasma aminopeptidases. In vivo, the intravenous administration of the tetrapeptide corrects the hypertension and the MgBD as well. The MgBD also occurs in type 2 diabetes mellitus and, thus, the decreased intracellular concentrations of Mg2+ and MgATP2- ions appear to be involved also in the cause of this disease, which is reputed to be the fifth most deadly disease in the world.
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PMID:Abnormal magnesium metabolism in etiology of salt-sensitive hypertension and type 2 diabetes mellitus. 1507 8

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 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 importance of magnesium intake in relation to the metabolic syndrome has been increasingly recognized. Magnesium is an essential mineral, critical for a number of metabolic functions in the human body. The major dietary sources of magnesium intake include whole grains, legumes, nuts, and green leafy vegetables. Animal studies indicate a pivotal role of magnesium in glucose homeostasis and insulin secretion and action. Experimental and clinical studies suggest that magnesium intake may be inversely related to the risk of hypertension and type 2 diabetes mellitus, and may decrease blood triglyceride and increase high-density lipoprotein cholesterol levels. The purpose of this brief review is to summarize the epidemiologic data relating magnesium to the metabolic syndrome and to discuss the potential mechanisms.
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PMID:Magnesium intake and the metabolic syndrome: epidemiologic evidence to date. 1767 97

Magnesium is an essential mineral and has been established as a cofactor for over 300 metabolic reactions in the body. Some research has indicated that lower intakes of magnesium and lower serum magnesium concentrations may lead to and are associated with the metabolic syndrome, insulin resistance, and/or type 2 diabetes mellitus. The goal of this review is to examine the research conducted on: 1) magnesium status, metabolic syndrome, insulin resistance, and type 2 diabetes mellitus, and 2) the effects of magnesium intake and/or supplementation on metabolic syndrome, insulin resistance, and type 2 diabetes mellitus. To make this review as current as possible, the majority of research articles reviewed were from 2000 to the present.
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PMID:Magnesium, the metabolic syndrome, insulin resistance, and type 2 diabetes mellitus. 1827 77


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