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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 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

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two aetiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilization, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons, i.e., non-insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing, particularly in neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism-the simplest marker of which is non-response to the dexamethasone suppression test-may include immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycaemia, hyperlipidaemia, atherosclerosis, and disturbances of mood and mental performance through accelerated hippocampal ageing particularly. It seems very important to point out that magnesium deficit and stress aggravate each other in a true 'pathogenic vicious circle', particularly in the stressful state of ageing. The importance of magnesium deficit in the aetiologies of insulin resistance, and the adrenergic, osseous, oncogenic, immune and oxidant disturbances of ageing is still uncertain. Oral physiological magnesium supplementation (5 mg Mg/kg/d) is the best diagnostic tool for establishing the importance of magnesium deficiency. Too few open and double blind studies on the effects of the treatment of magnesium deficiency and of magnesium depletion in geriatric populations have been done. Further study is necessary to assess the true place of magnesium deficit in the pathophysiology of ageing.
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PMID:Magnesium and ageing. II. Clinical data: aetiological mechanisms and pathophysiological consequences of magnesium deficit in the elderly. 815 90

Patients with diabetes mellitus were surveyed to determine magnesium utilization and supplementation patterns and the extent to which these patterns correlate with American Diabetes Association (ADA) consensus panel recommendations. Participating ADA member physicians were asked to enroll five or more patients with insulin-dependent diabetes mellitus (IDDM, or type I diabetes) or non-insulin-dependent diabetes mellitus (NIDDM, or type II diabetes) who were not currently receiving magnesium supplementation and who they believed required or could benefit from oral magnesium chloride administration. Data were then collected regarding specific patient characteristics (ie, current diabetes therapy and glucose control); concomitant diseases and cardiovascular medications; baseline serum magnesium level, if measured before initiating magnesium chloride supplementation; and magnesium chloride dosage and duration. A total of 199 patients with diabetes began treatment with magnesium chloride supplementation after enrollment by a specialist. The mean baseline serum magnesium level for patients with IDDM was 1.48 mg/dL and for patients with NIDDM was 1.44 mg/dL (normal range, 1.80 to 2.40 mg/dL). No differences in mean serum magnesium levels were observed between men and women and between those with IDDM and those with NIDDM. Glucose control, as measured by glycosylated hemoglobin Alc, did not correlate with magnesium serum levels. A concomitant cardiovascular disease was present in 70% of patients. In 78.3% of patients, supplementation was initiated because of low serum magnesium levels; in 21.7%, magnesium chloride therapy was initiated empirically. No correlation was found between serum magnesium levels and the prescribed dosage or the recommended duration of magnesium therapy. Patterns of magnesium utilization among survey respondents generally followed ADA consensus panel recommendations. A majority of diabetic patients who were given magnesium chloride supplementation had concomitant cardiovascular disease. Primary care physicians and cardiologists who treat large numbers of patients with diabetes and cardiovascular disease should be knowledgeable of the ADA consensus report because of the high prevalence of hypomagnesemia and because of the consequences of magnesium deficiency in these high-risk groups. To achieve successful long-term maintenance in these patients, additional physician education appears to be necessary regarding initial dosing strategies and recommended duration of supplementation.
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PMID:Magnesium utilization survey in selected patients with diabetes. 873 89

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two etiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilisation, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin-resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons: i.e. non insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing: mainly neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism--whose non response to dexamethasone suppression test appears the simplest marker--may concern immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycemia, hyperlipidemia, atherosclerosis, disturbances in mood and mental performances through accelerated hippocampal ageing particularly. Treatment of magnesium deficiency requires simple oral physiological magnesium supplementation. Treatment of the different types of magnesium depletion leads to a more or less specific control of pathophysiological disturbances of the required magnesium substrate. Open and double blind studies on the effects of the treatments of magnesium deficiency and of magnesium depletions in geriatic populations are too scarce. Further study is necessary to assess the accurate place of magnesium deficit in the physiopathology of ageing.
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PMID:Magnesium status and ageing: an update. 959 47

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

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.
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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 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 increasing evidence for the clinical relevance of altered magnesium metabolism to states of altered insulin resistance confirms the role of magnesium deficit as a possible underlying common mechanism of the "insulin resistance" of hypertension and altered glucose tolerance. The pioneer work of Lawrence M. Resnick and his group using the cellular ion-based approach that we are only partially presenting here has consistently contributed to the progress of the field, demonstrating (a) the critical importance of magnesium metabolism in regulating insulin sensitivity as well as vascular tone, and blood-pressure homeostasis; (b) that magnesium deficiency, defined on the basis of intracellular free magnesium levels, and or serum ionized magnesium is a common feature of both diabetic and hypertensive states as well as various other cardiovascular and metabolic processes and aging; (c) the ability of environmental factors such as dietary nutrient-sugar and mineral content to alter the set point of steady-state cell ion activity; and (d) that magnesium supplementation is indicated in conditions associated with magnesium deficit although well-designed therapeutic trials of magnesium in essential hypertension and type 2 diabetes mellitus are needed in the near future.
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PMID:Magnesium metabolism in hypertension and type 2 diabetes mellitus. 1766 14


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