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

Maternal and fetal magnesium homeostasis is reviewed. Current evidence suggests that pregnancy-associated growth is unlikely to cause maternal magnesium deficiency and that the case for magnesium supplementation during pregnancy is unproven. Similarly, data do not support the use of magnesium in prevention of preterm labor or its preferential use in tocolysis. Magnesium might have a role to play in the prevention/treatment of eclamptic seizures. Hypomagnesaemia occurs in poorly controlled diabetic pregnancy and may be part of the cause of the hypomagnesaemia in the infants of such mothers. Fetal magnesium homeostasis is poorly understood as is the mechanism of placental transfer. Data from the rat suggest that the bulk of maternofetal placental magnesium transfer occurs via a transcellular route utilising a Na+/Mg2+ exchanger and that maternofetal flux of magnesium is reduced in the presence of maternal diabetes mellitus. Further study of diabetic pregnancy will increase our understanding of magnesium homeostasis both in normal and abnormal pregnancy.
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PMID:Magnesium and pregnancy. 826 17

Magnesium (Mg) requirements depend on body weight. Recommended dietary allowances (RDA) are mostly given in absolute amounts and are mostly similar for adults, despite differences in body composition in the adult age range. We therefore studied the interrelations of 24 h urinary Mg excretion with body build and body composition indicators, as well as with factors potentially affecting the metabolism of Mg, among 520 elderly men and women seen in a nationwide survey. Mg intake data were also obtained in the Dutch Food Composition Survey amount 5898 subjects. The results showed lower mean Mg intake among elderly people (especially men) and positive associations of body weight and body height with urinary Mg excretion, but not when expressed per mmol of creatinine excreted. Mg excretion per mmol of creatinine was not associated with body weight, body height, body mass index or body fatness (women), suggesting that the amount of fat mass did not affect Mg excretion. Mg excretion was positively correlated with Mg intake, creatinine clearance, excretion of sodium, potassium and calcium, and coffee consumption, indicating interactions at the kidney level that may increase Mg losses. Elderly people using diuretics and/or anticholinergics and male diabetics had a higher mean Mg excretion per mmol of creatinine. The results show that, besides the Mg intake, several factors affect the urinary Mg excretion among elderly people. These factors were body build and body composition, dietary intake, drug use, kidney function, and diabetes. A quantification of the effects cannot be made yet, and controlled studies on those factors potentially affecting the requirement of Mg are needed.
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PMID:Body composition, health status and urinary magnesium excretion among elderly people (Dutch Nutrition Surveillance System). 829 95

The possibility that distinct genetic factors may concur, in association with diabetes, to increase susceptibility to vascular morbidity, including hypertension, has been evaluated in ninety-four normotensive insulin-dependent diabetic patients by testing both the frequency and prevalence of hypertension in parents and by measuring membrane red blood cell enzyme activities. Parental hypertension was present in a significantly higher proportion of diabetic compared to control subjects. A significant decrease in basal membrane red blood cell (Na(+)-K+), (Mg2+) and (Ca2+) ATPase activities was also related to the disease and was apparently uninfluenced by short--or long term metabolic control. In contrast with what was observed in the control group, sex caused in diabetic subjects significant variations in red blood cell enzyme activities, with women showing the lowest mean basal values of all enzyme activities. Parental hypertension turned out to be an independent risk factor in significantly reducing red blood cell enzyme activities both in diabetic and control subjects. However, whereas in diabetic subjects sex interacted strongly with parental hypertension in causing reduction of enzyme activities, in controls the effect of parental hypertension was sex-independent and significantly reduced basal enzyme activities, thus rendering subjects similar to diabetics. It is concluded that both sex and parental hypertension in association with diabetes, are predictors of further damage to red blood cell enzyme activities, which may thus be linked to increased risk of susceptibility towards vascular complications.
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PMID:Sex and parental hypertension as predictors of worsened red blood cell membrane enzyme activities in type 1 insulin-dependent diabetic subjects. 838 3

The activity of adipose tissue hormone-sensitive lipase in animals with hyperinsulinemia has been reported to be increased compared with that in control animals. We examined whether this results from a direct effect of insulin on the tissue and whether it is accompanied by alteration in the regulation of lipolysis. When rat epididymal fat pads are incubated in culture medium with bovine serum albumin for 2-4 h with 2 ng/ml or 50 microU/ml of insulin, hormone-sensitive lipase activity in the postmicrosomal supernatant fraction after acid precipitation and activation with ATP-Mg2+ increases significantly compared with preparations from tissues incubated with the vehicle. The specific activities of hormone-sensitive lipase in sonicates of adipocytes after primary culture with insulin at concentrations from 10 to 4000 ng/ml (250 microU to 100 mU/ml) increase in an insulin-dose-related manner. Lipolysis in response to 10(-7) M isoproterenol also increases in an insulin-dose-dependent manner. Enhancement of isoproterenol-mediated lipolysis is not attributable to a difference in the triglyceride content of the cells. Lipolysis caused by the beta-agonist could be completely blocked by the simultaneous presence of insulin in both control and insulin-treated cells reflecting normal responsiveness of both types of cells to the acute effect of insulin. Although an increase in lipolysis is seen with norepinephrine and growth hormone after insulin treatment, other lipolytic agents such as ACTH, thyrotropin, and glucagon evoke similar responses in insulin-treated and control cells. The simultaneous presence of growth hormone and insulin during the 16-h culture results in additive effects on the subsequent response of the cells to 10(-7) M isoproterenol compared with the responses of the cells cultured with each hormone alone. beta-Agonist-mediated cAMP accumulation in the presence of Ro-20.1724, a specific phosphodiesterase inhibitor, is significantly higher in cells cultured in the presence of insulin than in control cells. Forskolin (1-25 microM) increases the lipolytic responses of insulin-treated cells compared with control cells, but the maximal response of the insulin-treated cells to forskolin is lower than that to isoproterenol. We conclude that changes produced by chronic insulin treatment involve more than one site along the lipolytic cascade.
Diabetes 1993 Oct
PMID:Chronic exposure of rat fat cells to insulin enhances lipolysis and activation of partially purified hormone-sensitive lipase. 839 27

Alterations in intracellular cation concentrations in the kidney during hyperglycemia may play a role in a number of complications associated with diabetes mellitus such as renal hypertrophy and hypertension. In this study, we have investigated the effect of 25 mM glucose on intracellular pH and free Mg2+, free Ca2+, and Na+ concentrations in the perfused kidneys of Sprague-Dawley rats using 31P, 19F, and 23Na triple-quantum filtered NMR. No significant alteration occurred in the intracellular free Mg2+ concentration, pH, or ATP concentration during hyperglycemia. However, a sizable (approximately 50%) increase in the intracellular Na+ concentration was inferred from 23Na triple-quantum filtered NMR after 30-45 min of perfusion with 25 mM glucose. Intracellular free Ca2+, measured to be 390 +/- 15 nM at 5 mM glucose, increased significantly (95%; p < 0.001) to a value of 765 +/- 28 nM after 30 min of perfusion with 25 mM glucose. This effect of glucose was reversible. Only small increases (< or = 20%) in free Ca2+ were found with addition of comparable concentrations of a nontransportable sugar (20 mM mannitol), indicating that glucose entry into the cell (through the Na+/glucose cotransporter) plays a role in causing the free Ca2+ increase. No effect on free Ca2+ was however, seen with 1 mM ouabain, which caused a sizable increase in intracellular Na+, indicating that Na+/Ca2+ exchange does not play a significant role in the maintenance of low intracellular free Ca2+ in the kidney and that the observed increase in free Ca2+ is probably due to a decrease in the Ca2+/Mg(2+)-ATPase activity during hyperglycemia. Increased concentrations of Na+ and free Ca2+ during hyperglycemia may be involved in the mechanism of renal hypertrophy and hypertension, frequently associated with diabetes mellitus.
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PMID:NMR studies of the effect of hyperglycemia on intracellular cations in rat kidney. 841 77

Ischemia is often implicated as a cause of acute renal failure. We have investigated the effect of various concentrations of extracellular Mg2+ on the post-ischemic recovery of ATP and low intracellular Na+ in the isolated perfused rat kidney using 31P and triple-quantum filtered (TQ) 23Na-NMR spectroscopy. Following a 1 h period of stopped flow ischemia, the kidneys exposed to 0.3 mM Mg2+ throughout the experiment exhibited a significantly (p < 0.05) decreased post-ischemic fractional recovery of ATP (56 +/- 7%) as well as a significantly (p < 0.05) increased accumulation of P(i) (250 +/- 30%) as compared to kidneys exposed to 1.2 mM Mg2+ throughout (88 +/- 5% recovery of [ATP] and 158 +/- 8% accumulation of [P(i)]). Kidneys exposed to 0.3 mM Mg2+ during the pre-ischemic and ischemic periods but to 1.2 mM Mg2+ during reperfusion also showed better recovery of ATP (83 +/- 6%) and lower accumulation of P(i) (143 +/- 8%) compared to kidneys exposed to low Mg2+ (0.3 mM) throughout the experiment. Measurements of the 23Na TQ signal following ischemia-reperfusion revealed that kidneys exposed to 1.2 mM Mg2+ exhibited significantly improved maintenance of low intracellular Na+ as compared to those exposed to 0.3 mM Mg2+ ([Na+]i = 107 +/- 7% in 1.2 mM Mg2+ vs. 152 +/- 3% in 0.3 mM Mg2+). No significant difference was found in the pre-ischemic basal intracellular free Ca2+ level (as measured by 19F-NMR in combination with 5 FBAPTA) between kidneys perfused with 1.2 mM and 0.3 mM Mg2+, and comparable depletion of ATP occurred during ischemia under both experimental conditions. These data indicate that increased extracellular Mg2+ has a protective effect against post-ischemic damage, probably related to its role in resynthesis of ATP during post-ischemic reperfusion. Our results would imply a greater vulnerability of the kidney to ischemic damage in hypomagnesemic clinical conditions such as alcoholism and diabetes.
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PMID:NMR studies of the effect of Mg2+ on post-ischemic recovery of ATP and intracellular sodium in perfused kidney. 854 43

Magnesium depletion is more common than previously thought. It seems to be especially prevalent in patients with diabetes mellitus. It is usually caused by losses from the kidney or gastrointestinal tract. A patient with magnesium depletion may present with neuromuscular symptoms, hypokalemia, hypocalcemia, or cardiovascular complication. Physicians should maintain a high index of suspicion for magnesium depletion in patients at high risk and should implement therapy early.
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PMID:Disorders of magnesium metabolism. 857 13

GENETIC PREDISPOSITION: Insulin resistance and reactive hyperinsulinemia occur not only with obesity, impaired glucose tolerance or non-insulin-dependent (type 2) diabetes mellitus, but also in many non-obese, non-diabetic patients with essential hypertension and their currently normotensive, lean, young offspring, as well as in some other conditions known to promote hypertension. Insulin resistance impairs glucose tolerance, while insulin resistance and/or hyperinsulinemia promote dyslipidemia, body fat deposition and probably atherogenesis. Therefore, the common coexistence of a genetic predisposition for hypertension with insulin resistance helps to explain the frequent, although temporally often dissociated, occurrence of hypertension together with dyslipidemia, obesity and type 2 diabetes in a given patient. INSULIN RESISTANCE AND HYPERINSULINEMIA AS SLOW PRESSOR MECHANISMS: In the pathogenesis of hypertension, inappropriate vasoconstriction (due to an imbalance of vasoactive substances and/or raised cytosolic calcium) and/or structural vasculopathy is particularly important. Among the mosaic of assumed pressor mechanisms, distinct Na+ retention is almost invariably involved in diabetes mellitus, while sympathetic activation tends to occur in essential hypertension, particularly in association with obesity. Insulin resistance may develop as a consequence of an intracellular excess of Ca2+ or a decrease in Mg2+, an impaired insulin-mediated rise in skeletal muscle blood flow, increased sympathetic activity or excess body weight. Acute hyperinsulinemia causes arterial vasodilation on one hand and increases sympathetic activity and renal Na+ reabsorption on the other. Chronically, hyperinsulinemia may promote cardiovascular muscle cell proliferation and atherogenesis, while insulin resistance may be associated with certain transmembraneous cation transporters, leading to an increase in cytosolic Ca2+. Hyperinsulinemia and/or insulin resistance may also be associated with an increased blood pressure sensitivity to high salt intake. In the mosaic of many different blood pressure-raising mechanisms, insulin resistance and/or hyperinsulinemia is likely to represent an amplifying slow or very slow pressor factor.
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PMID:Insulin resistance and hyperinsulinemia in hypertension. 857 90

Magnesium(Mg)-deficiency, whether dietary or an effect of a clinical condition such as diabetes, results in a variety of cardiovascular pathologies. Substance P (SP) has been implicated in the induction of cardiac focal inflammatory lesions that occur during Mg-deficiency. Blockade of SP receptors results in a significant reduction in the incidence of lesion formation. In an effort to identify potential endogenous cell populations of the heart, which may play a role in SP-dependent lesion formation, film- and light-microscopic autoradiography were used to map the distribution of specific SP binding sites in frozen sections of the normal rat heart and adjacent great vessels. Binding was assessed with 0.1 nM I-125 Bolton-Hunter labelled SP in the absence (total binding) or presence (non-specific binding) of excess unlabelled SP, prolactin, or L-703,606, a non-peptide antagonist of SP receptors. Film autoradiograms revealed prominent small foci of intense autoradiographic reactions dispersed intermittently around the periphery of the great vessels and coronary arteries, among the interstitial connective tissue of the heart, and along the cusps of the cardiac valves. Excess unlabelled SP caused a significant reduction (97.7% displacement; P < 0.001) in the focal autoradiographic reactions. L-703,606 caused a similar reduction in SP binding (97.3% displacement; P < 0.001), while prolactin had no statistically significant effect on the binding of radiolabelled SP. Light-microscopic autoradiograms revealed that the SP binding sites occurred within clusters of connective tissue cells or in rarely observed parasympathetic ganglia. No evidence was found to suggest the presence of SP receptors on endothelial cells, cardiac muscle fibers, or smooth muscle fibers. The connective tissue cells which bound SP within the heart will likely include types that are susceptible to SP activation and thus may play a role in initiation of the focal inflammation characteristic of Mg-deficiency.
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PMID:Distribution of specific substance P binding sites in the heart and adjacent great vessels of the Wistar white rat. 864 67

In this review, a rationale is presented for how hypercholesterolemia, hypertension, diabetes mellitus, end-stage renal disease, renal dialysis, and prolonged stress can all lead to atherosclerosis, ischemic heart disease, and stroke. The data indicate that Mg deficiency caused either by poor diet and/or errors in Mg metabolism may be a missing link between diverse cardiovascular risk factors and atherosclerosis. Data from our laboratories and others indicate that reduction in extracellular and intracellular free Mg ions (Mg2+) can induce an entire array of pathophysiological phenomena known to be important in atherogenesis, that is, vasospasm, increased vascular reactivity, elevation in [Ca2+]i, formation of proinflammatory agents, oxygen radicals, platelet aggegation, reduction in cardiac bioenergetics, cardiac failure, oxidation of lipoproteins, gender-related modulation of endothelial-derived relaxing factor/NO, changes in membrane fatty acid saturation, changes in membrane plasmalogens and N-phospholipids (suggesting changes in intracellular phospholipid signals), and probably transcription factors.
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PMID:Magnesium and cardiovascular biology: an important link between cardiovascular risk factors and atherogenesis. 886 81


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