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Query: UMLS:C0085580 (essential hypertension)
 14,686 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 levels have been shown to be associated with elevated blood pressure (BP), endothelial dysfunction, insulin resistance, vascular calcification, inflammation, and atherosclerosis. It was also demonstrated that patients with hypertension have increased inflammation, insulin resistance, and endothelial dysfunction. However, the relationship between magnesium, ambulatory BPs, and central hemodynamic parameters were not evaluated extensively. Serum magnesium levels, ambulatory blood pressures, augmentation index (Aix), pulse wave velocity, total peripheral resistances, and cardiac output were measured for all patients. In total, 184 essential hypertension patients were enrolled. In univariate analysis, magnesium levels were correlated with hemoglobin (r = +0.155; P = .037), albumin (r = +0.180; P = .018), pulse pressure (daytime; r = -0.170; P = .021), pulse pressure (24-hour; r = -0.156; P = .035), Aix (daytime; r = -0.223; P = .002), Aix (nighttime; r = -0.169; P = .022), and Aix (24-hour; r = -0.247; P = .001). In regression analysis, magnesium levels were independently and conversely associated with daytime Aix (P < .0001), nighttime Aix (P = .019), and 24-hour Aix (P < .0001). We suggest that magnesium levels were associated with Aix but not with total peripheral resistances, pulse wave velocity, cardiac output, and central BPs. The unique mechanisms related with magnesium and Aix but not shared by other central parameters needs to be determined.
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PMID:The relationship between magnesium and ambulatory blood pressure, augmentation index, pulse wave velocity, total peripheral resistance, and cardiac output in essential hypertensive patients. 2450 35


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