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PubMed1984

[Magnesium deficiencies in cardiovascular diseases].

Plasma (pl), red blood cell (ery) and urinary magnesium (Mg) concentrations were measured by spectrophotometry in over 300 patients at the Cardiology Department of Broussais Hospital. Other biological parameters, including pl and ery potassium, calcium and phosphate concentrations were measured simultaneously. In a control group (54 subjects) the mean pl Mg was 0,851 mmol/l in men and 0,819 mmol/l in women; mean ery Mg was 2,12 mmol/l and 2,09 mmol/l respectively. Magnesium depletion was observed in several pathological cardiovascular conditions: -- mitral valve prolapse: the Mg levels were significantly lower in women (19 cases) (pl Mg 0,740 mmol/l; ery Mg 1,83 mmol/l: p less than 0,001); the deficit was less pronounced in men: pl Mg 0,829 mmol/l, p less than 0,01, and ery Mg 2,01 mmol/l (NS); -- recurrent junctional tachycardia (21 cases): the Mg levels were significantly lower than normal: pl Mg = 0,796 mmol/l in men and 0,763 mmol/l in women; ery Mg = 1,93 and 1,88 mmol/l, respectively; -- coronary insufficiency (86 cases): pl Mg = 0,821 mmol/l in men and 0,768 mmol/l in women (p less than 0,001). In a subgroup with coronary spasm (22 cases), the mean ery Mg was decreased (2,01 mmol/l, p less than 0,05); -- unstable or labile hypertension (24 cases): the decrease was significant, especially in women (pl Mg = 0,796 mmol/l, ery Mg = 1,88 mmol/l). These magnesium deficits were sometimes associated with a low pl Ca, and often associated with a low ery K although pl K was usually raised. In some privileged cases of cardiac arrhythmia and coronary spasm, intravenous Mg repletion was beneficial but did not affect plasma concentrations. The role of magnesium depletion in cardiovascular disease remains obscure and requires further study.

Adolescent↗
PubMed1994

Magnesium deficiency and alcohol intake: mechanisms, clinical significance and possible relation to cancer development (a review).

A comprehensive and critical review of the evidence relating magnesium (Mg) deficiency to alcohol consumption reveals several important types of interactions. First, alcohol acts acutely as a Mg diuretic, causing a prompt, vigorous increase in the urinary excretion of this metal along with that of certain other electrolytes. Second, with chronic intake of alcohol and development of alcoholism, the body stores of Mg become depleted. During the late stages of alcoholism, the urinary excretion of Mg may become diminished as a physiological response to reduced intake and reduction of body stores. A number of aspects of the clinical syndrome of alcoholism contribute to and intensify that already existing reduction in body Mg stores. Third, a number of manifestations of alcoholism are believed due to effects of Mg deficiency, and some therapeutic benefit has been suggested from treatment of alcoholic patients with Mg. Finally, relatively little attention has been paid to the possible value of Mg administration as a preventive measure to forestall or minimize the deleterious effects of chronic use of alcohol or to prevent the development of cancer than can occur in this setting.

Alcoholism↗
PubMed1979

Evidence for skeletal resistance to parathyroid hormone in magnesium deficiency. Studies in isolated perfused bone.

Hypocalcemia during magnesium (Mg) depletion has been well described, but the precise mechanism(s) responsible for its occurrence is not yet fully understood. The hypocalcemia has been ascribed to decreased parathyroid hormone (PTH) secretion as well as skeletal resistance to PTH. Whereas the former is well established, controversy exists as to whether or not Mg depletion results in skeletal resistance to PTH. These studies examine the skeletal response to PTH in normal dogs and dogs fed a Mg-free diet for 4-6 mo. Isolated tibia from normal (serum Mg 1.83+/-0.1 mg/100 ml) and experimental dogs (serum Mg 1.34+/-0.15 mg/100 ml) were perfused with Krebs-Henseleit buffer during a constant infusion of 3 ng/ml of synthetic bovine PTH 1-34 (syn b-PTH 1-34). The arteriovenous (A-V) difference for immunoreactive PTH (iPTH) across seven normal bones was 37.5+/-3%. In contrast, the A-V difference for iPTH was markedly depressed to 10.1+/-1% across seven bones from Mg-depleted dogs. These findings correlated well with a biological effect (cyclic AMP [cAMP] production) of syn b-PTH 1-34 on bone. In control bones, cAMP production rose from a basal level of 5.8+/-0.2 to 17.5+/-0.7 pmol/min after syn b-PTH 1-34 infusion. In experimental bones, basal cAMP production was significantly lower than in controls, 4.5+/-0.1 pmol/min, and increased to only 7.1+/-0.4 pmol/min after syn b-PTH 1-34 infusion. Even when PTH concentrations were increased to 20 ng/ml, cAMP production by experimental bones was lower than in control bones perfused with 3 ng/ml. Histological examination of bones from Mg-deficient dogs showed a picture compatible with skeletal inactivity. These studies demonstrate decreased uptake of iPTH and diminished cAMP production by bone, which indicates skeletal resistance to PTH in chronic Mg deficiency.

Animals↗
PubMed1996

Change in glucose homeostasis in rats by long-term magnesium-deficient diet.

It is widely known that hypomagnesemia is one of the symptoms observed in diabetic patients. This study was performed to assess the effect of chronic magnesium (Mg) deficiency on glucose metabolism in rats. Male Sprague-Dawley rats (at the age of four weeks) were given a Mg-deficient diet or a control diet for two to eight weeks. The rats were orally administered sucrose solution (2 g/kg BW) every two weeks, and blood was drawn from a tail vein before and 15 min after sucrose loading to determine the concentrations of blood glucose and plasma insulin. At the same time, other rats in a non-fasted condition were sacrificed by decapitation (rats sacrificed at eight weeks were rats used for sucrose loading). The epididymal fat pads were immediately removed and adipocytes were isolated. The amount of glucose transporter 4 (GLUT4) in the plasma membranes and low-density microsomal membranes prepared from the adipocytes was measured by immunoblotting to estimate the influence of chronic Mg deficiency on glucose metabolism at the cellular level. In addition, plasma biochemical parameters and muscle mineral contents were also evaluated. The glucose concentration in fasted blood was significantly lower in Mg-deficient rats than in control rats throughout the experiment period. The feeding of a Mg-deficient diet also attenuated the response of blood glucose and plasma insulin: the glucose level in blood tended to be lower in Mg-deficient rats at 15 min after oral sucrose administration, and the difference was significant at two and eight weeks. The plasma insulin level in Mg-deficient rats was also lower, reaching a significant difference at two weeks. When animals were sacrificed in a non-fasted condition at 2-week intervals, the plasma glucose level was also significantly decreased in Mg-deficient rats as compared to control rats throughout the experiment period. The plasma insulin level in non-fasted Mg-deficient rats was also significantly decreased at two and six weeks. The Mg-deficient diet increased plasma triglyceride, but the difference was significant only at four weeks, and plasma cholesterol remained unchanged. The plasma Mg level was markedly lower in Mg-deficient rats throughout the experiment period. In Mg-deficient rats, the Mg content in muscle was significantly reduced at two and eight weeks, whereas the calcium and sodium contents were significantly increased throughout the experiment period. In Mg-deficient rats, the degree of translocation of GLUT4 to plasma membranes in the adipocytes stimulated by insulin was reduced only at eight weeks. In conclusion, since fasted and non-fasted blood glucose levels and the response of blood glucose to sucrose loading were decreased in Mg-deficient rats, it is suggested that Mg deficiency induces changes in the glucose metabolism via impaired glucose absorption in the intestine or an altered glucose uptake in the liver and/or peripheral tissues.

Adipocytes↗
PubMed1995

Magnesium deficiency enhances basal glucose disposal in the rat.

To investigate the contribution of hepatic and peripheral tissues to the enhanced glucose disposal rate (Kg) observed in magnesium (Mg)-deficient rats, euglycemic-hyperinsulinemic clamps were performed with continuous infusion of [3-3H]glucose and three insulin infusion rates, 1, 8, and 16 microU.kg-1.min-1. Moderately Mg-deficient (Mg-, 4.2 microM Mg/g diet) and Mg-adequate (Mg+, 16.7 microM Mg/g diet) Sprague-Dawley rats were studied after 3 wk of dietary treatment. Growth, fasting glucose, and insulin concentrations were not affected by dietary treatment. Basal hepatic glucose output (HGO) and glucose disposal (Rd) were increased by 24% in Mg- rats (P < 0.001). After 1 microU insulin.kg-1.min-1 infusion, Rd and the glucose infusion rate that maintained euglycemia were significantly increased in Mg- rats by 24 and 46%, respectively. However, when the increase in Rd above baseline was examined, no significant differences were observed. Therefore, the increased basal glucose disposal observed in Mg- rats may be mediated by noninsulin-dependent mechanisms. Insulin suppression of HGO during 1 microU insulin.kg-1.min-1 infusion was greater in Mg- rats (43%) compared with Mg+ rats (27%, P < 0.05). In conclusion, the increased Kg observed in Mg- rats is likely to be caused by an increase in noninsulin-mediated glucose uptake and an enhancement of hepatic insulin sensitivity.

Animals↗
PubMedDate not supplied

Magnesium deficiency impairs rat soleus muscle glucose utilization and insulin sensitivity.

Insulin resistance (IR), probably a common pathway of atherosclerosis development in various diseases, was suggested to be related to magnesium (Mg) deficiency. The in vivo observations required an in vitro extension. The study was performed on isolated rat soleus muscle incubated in Ringer bicarbonate with/without Mg. Mg deficiency inhibited basal, insulin- and tolbutamide-stimulated glucose utilization. Insulin-stimulated glucose utilization was inhibited even in the case that insulin was given to rats before sacrifice. Similar inhibition of glucose utilization was found in Ca deficiency and the simultaneous lack of Mg had no additive effect. It is concluded that Mg deficiency inhibits glucose utilization at the level of Ca mediation of glucose transport regulation.

Animals↗