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

Evidence is reviewed supporting the presence of an inherited structural defect in the plasma membranes of somatic cells of humans who have type 2 diabetes mellitus and sodium-sensitive essential hypertension. This magnesium-binding defect (MgBD) consists of a decreased content of tightly bound Mg2+ ion in the cell membrane and limits the amount of Mg2+ that enters the cell, some of which combines with ATP4-, produced by the cell, to form MgATP2-, the currency of metabolic energy. Consequently, in both prediabetes and overt diabetes, the intracellular concentration of the interdependent Mg2+ and MgATP2- ions is significantly less than normal. These 2 ions are required as cofactors and (or) substrates for some 300 enzyme systems in human metabolism, many of which are involved with insulin. Thus the decreased activities of particular ones of these enzyme systems due to the decreased intracellular [Mg2+] and its dependent [MgATP2-] are responsible for (i) insulin resistance and (ii) decreased insulin secretion and (or) production, the 2 pathophysiological processes required for the occurrence of type 2 diabetes mellitus. These 2 processes can account for all of the morbid symptoms associated with this disease. Thus, the decreased intracellular concentration of the interdependent Mg2+ and MgATP2- ions constitutes the etiology of genetic predisposition to type 2 diabetes mellitus and can be corrected by 2 identified peptide Mg2+-binding promoters that are derived from the carboxyl terminal of the tachykinin substance P and occur in normal blood plasma. Decreased intracellular [Mg2+] and [MgATP2-] can also result from a dietary deficiency of magnesium or from an abnormal accumulation of saturated fatty acids in cell membranes, which inhibits the entrance of Mg2+ into the cell; thus it is also the etiology not only of diabetes caused by magnesium deficiency, but also of the "lipotoxic" type 2 diabetes mellitus. Although these pathologies cannot be corrected by the Mg2+-binding promoters, they can be corrected, respectively, by dietary magnesium supplementation or by exercise plus dietary caloric and lipid restriction. Theoretically, the disease syndrome containing type 2 diabetes mellitus may involve approximately 30% of the population.
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PMID:Evidence that the etiology of the syndrome containing type 2 diabetes mellitus results from abnormal magnesium metabolism. 1841 43

Magnesium is the fourth most abundant cation in the body and plays an important physiological role in many of its functions. It plays a fundamental role as a cofactor in various enzymatic reactions involving energy metabolism. Magnesium is a cofactor of various enzymes in carbohydrate oxidation and plays an important role in glucose transporting mechanism of the cell membrane. It is also involved in insulin secretion, binding, and activity. Magnesium deficiency and hypomagnesemia can result from a wide variety of causes, including deficient magnesium intake, gastrointestinal, and renal losses. Chronic magnesium deficiency has been associated with the development of insulin resistance. The present review discusses the implications of magnesium deficiency in type 2 diabetes.
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PMID:Implications of magnesium deficiency in type 2 diabetes: a review. 1962 3

Hypomagnesemia is common in hospitalized patients, especiaLLy in the eLderLy with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with the risk of hypertension, type 2 diabetes mellitus, increased mortality from all cause and CAD. Higher magnesium intake, however, has been associated with a Lower risk of developing metabolic syndrome, a problem which exists in 25% of American adults. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves human endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially provides magnesium with physiologic and natural effects similar to adenosine-diphosphate inhibitors, such as clopidogrel. Data on magnesium supplementation in patients with acute myocardial infarction (AMI) are conflicting. ALthough a number of relatively small randomized cLinicaL trials have demonstrated a remarkable reduction in mortality when magnesium is administered to relativeLy high risk AMI patients, two recently published large-scale randomized cLinical trials (the Fourth International Study of Infarct Survival and Magnesium in Coronaries) failed to show any superiority of intravenous magnesium over placebo. Furthermore, the theoretical potential benefits of magnesium supplementation as a cardioprotective agent in CAD patients, its relatively low cost, easy administration, and relatively insignificant adverse effects, gives magnesium a place in treating CAD patients, especially those at high-risk and in life-threatening ventricular arrhythmias, such as Torsades de Points and intractable ventricular tachycardia.
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PMID:[Body magnesium--the spark of life]. 2144 56

Type 2 diabetes mellitus can be defined as a conformational disease since a beta cell producing protein called amylin undergoes a change in the tertiary structure followed by self-aggregation and deposition. Amylin deposition causes destruction of pancreatic beta-cells. The aim of this study was to investigate whether different concentrations of magnesium and aluminium alter amylin conformation under near-physiological circumstances. Conformational variations were monitored by fluorescent method before and after incubation by shaker incubator in 37 degrees C by LS55 spectrofluorometer instrument. This in vitro study showed that magnesium had contradictory effects on amylin folding and these effects were magnesium concentration dependent. Magnesium with concentration of 1 to 1.5 mM had inhibitory effect but in 2.5 to 3.5 microM promoted amylin misfolding significantly (p < 0.05). The obtained data also demonstrated that aluminium with concentrations of 5, 10 and 20 microM had stimulatory effects on formation of beta-amyloid sheet significantly (p < 0.05). It may be concluded that islet amyloid misfolding and cytotoxicity to beta-cells might be magnesium dose dependent in diabetic patients.
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PMID:To study various concentrations of magnesium and aluminium on amylin hormone conformation. 2223 7

Magnesium (Mg) , one of the fundamental minerals acting the co-factor of about 300 kinds of enzymes and natural Ca channel blocker, plays an important role of cardiovascular, neurological, and metabolic functions in physiological, and pathophysiological conditions. Common abnormal Mg metabolism is an absolute or relative deficiency of Mg due to an attenuated Mg intake and an enhanced urinary Mg excretion, particularly in the metabolic syndrome (MetS) , type 2 diabetes (DM) , chronic heart failure (CHF) and hemodialysis (HD) patients with diabetes. It has been reported the Mg deficiency relating to enhanced risk of MetS and type 2 DM, and to fatal cardiac events in CHF and an atherosclerotic, vascular calcification in HD patients. On the otherhand, severe and fatal hypermagnesemia is very rare, except for the condition associated with high dose administration of Mg, renal failure and an abnormally enhanced Mg absorption from damaged intestine in the mesenteric ischemia/infarction, severe constipation or ileus. In this paper, we conduct to review and discuss the pathophysiological and pathogenetical role of the abnormal Mg metabolism focused on Mg deficiency, and the protective and therapeutic significance of Mg administration in the MetS, type 2 DM, CHF and diabetic HD patients.
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PMID:[Abnormalities of magnesium (Mg) metabolism and therapeutic significance of Mg administration in patients with metabolic syndrome, type 2 diabetes, heart failure and chronic hemodialysis]. 2284 58

Magnesium is the fourth most abundant mineral and the second most abundant intracellular divalent cation and has been recognized as a cofactor for >300 metabolic reactions in the body. Some of the processes in which magnesium is a cofactor include, but are not limited to, protein synthesis, cellular energy production and storage, reproduction, DNA and RNA synthesis, and stabilizing mitochondrial membranes. Magnesium also plays a critical role in nerve transmission, cardiac excitability, neuromuscular conduction, muscular contraction, vasomotor tone, blood pressure, and glucose and insulin metabolism. Because of magnesium's many functions within the body, it plays a major role in disease prevention and overall health. Low levels of magnesium have been associated with a number of chronic diseases including migraine headaches, Alzheimer's disease, cerebrovascular accident (stroke), hypertension, cardiovascular disease, and type 2 diabetes mellitus. Good food sources of magnesium include unrefined (whole) grains, spinach, nuts, legumes, and white potatoes (tubers). This review presents recent research in the areas of magnesium and chronic disease, with the goal of emphasizing magnesium's role in disease prevention and overall health.
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PMID:Magnesium in disease prevention and overall health. 2367 7

We have evaluated the effect of magnesium valproate (210 mg/kg/day, p.o.) in type 2 diabetes induced cardiovascular complications induced by streptozotocin (STZ, 90 mg/kg, i.p.) in neonatal wistar rats. Various biochemical, cardiovascular and hemodynamic parameters were measured at the end of 8 weeks of treatment. STZ produced significant hyperglycaemia, hypoinsulinemia and dyslipidemia, which was prevented by magnesium valproate treatment. STZ produced increase in Creatinine Kinase, C-reactive protein and lactate dehydrogenase levels and treatment with magnesium valproate produced reduction in these levels. STZ produced increase in cardiac and LV hypertrophy index, LV/RV ratio, LV collagen deposition and LV cardiomyocyte diameter which were decreased by magnesium valproate treatment. Magnesium valproate also prevented STZ induced hemodynamic alterations and oxidative stress. These results were further supported by histopathological studies in which magnesium valproate showed marked reduction in fibrosis and cardiac fiber disarray. In conclusion, our data suggests that magnesium valproate is beneficial as an anti-diabetic agent in type-2 diabetes mellitus and also prevents its cardiac complications.
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PMID:Cardioprotective effects of magnesium valproate in type 2 diabetes mellitus. 2453 Apr 14

Magnesium (Mg(2+)) deficiency is common in metabolic disorders such as obesity, type 2 diabetes, and insulin resistance. These disorders are also associated with a high incidence of cancer. Mg(2+) is the regulator par excellence of metabolism, largely through its role as a cofactor for all phosphoryl transfers in the cell. Because Mg(2+) deficiency inhibits energy production it might be expected to inhibit tumor production. However, the high incidence of cancer in metabolic disorders makes that seem unlikely. In order to understand this seeming paradox, it is important to understand the regulatory role of Mg(2+) in normal and neoplastic cells. Free Mg(2+) is the primary regulator of glycolysis and the Krebs cycle. It also acts as a second messenger for growth factors in regulating protein synthesis. Varying Mg(2+) concentrations result in the same set of coordinated responses as varying serum concentrations. Selection by serial rounds of high cell density or reduced serum concentration at low cell density results in progressive stages of field cancerization. Highly transformed cells proliferate in much lower concentrations of Mg(2+) and grow to much higher saturation densities than normal cells. It remains to be seen whether reduction in Mg(2+) in sparse, exponentially proliferating cultures selects for increases in saturation density and transformed foci.
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PMID:The paradox of the contrasting roles of chronic magnesium deficiency in metabolic disorders and field cancerization. 2556 Feb 38

Magnesium is actively involved in a number of metabolic reactions as an important co-factor, with special emphasis on carbohydrate metabolism. After a brief overview of the regulation of intra- and extracellular magnesium, the present review first describes the regulatory role of magnesium in important metabolic pathways involved in energy metabolism and glycaemic control. Next the clinical significance of hypomagnesaemic conditions with regard to the management of glucose in prediabetic stages, such as insulin resistance/impaired glucose tolerance and in type 2 diabetes mellitus are characterized. Cross-sectional as well as longitudinal studies suggest that a reduced dietary magnesium intake serves as a risk factor for the incidence of both impaired glucose regulation and type 2 diabetes. Mechanisms that might be responsible for diabetes-associated hypomagnesaemia are discussed. Furthermore, the role of hypomagnesaemia in the development and progression of chronic diabetic complications are addressed. Finally, the available literature on the effects of magnesium supplementation on glycaemic control parameters during prediabetic conditions (preventive approach) as well as type 2 diabetes mellitus (therapeutic approach) are reviewed systematically. There is considerable evidence that chronic magnesium supplementation may delay the progression from impaired glucose regulation to type 2 diabetes; however, the effects of oral magnesium supplementation as an adjunct therapy for type 2 diabetes are quite heterogeneous with respect to the various measures of glycaemic control. The results of this review suggest a requirement for critical consideration of the pros and cons of magnesium replacement therapy, based on variables such as magnesium status, stage of disease and glycaemic control.
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PMID:Magnesium and disturbances in carbohydrate metabolism. 2597 9

Observational studies between magnesium int- ake and risk of type 2 diabetes yielded inconsistent results. We conducted a system literature search of PubMed database through March 2015 for prospective cohort studies of magnesium intake and type 2 diabetes risk. Study-specific results were pooled in a random-effects model. Subgroup and sensitivity analysis were performed to assess the potential sources of heterogeneity and the robustness of the pooled estimation. Generalized least squares trend estimation was used to investigate the dose-response relationship. A total of 15 papers with 19 analyses were identified with 539,735 participants and 25,252 incident diabetes cases. Magnesium intake was associated with a significant lower risk of type 2 diabetes (RR: 0.77; 95% CI: 0.71-0.82) for the highest compared with lowest category. This association was not significantly modified by the pre-specified study characteristics. In the dose-response analysis, a magnesium intake increment of 100 mg/day was associated with a 16% reduction in type 2 diabetes risk (RR: 0.84; 95% CI: 0.80-0.88). A nonlinear relationship existed between magnesium intake and type 2 diabetes (P-nonlinearity=0.003). This meta-analysis further verified a protective effect of magnesium intake on type 2 diabetes in a nonlinear dose-response manner.
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PMID:Nonlinear Reduction in Risk for Type 2 Diabetes by Magnesium Intake: An Updated Meta-Analysis of Prospective Cohort Studies. 2624 37


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