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PubMed1987

Dietary calcium and phosphorus and seizure susceptibility of magnesium deficient rats.

Convulsions are characteristic of magnesium deficiency and hypocalcemia. In this study, weanling rats were fed magnesium deficient diets with varying concentrations of calcium and phosphorus. Diets were either normal (Mg =) or low (Mg-) in magnesium and were either low (Ca- or P-), normal (Ca = or P =) or high (Ca+ or P+) in calcium or phosphorus. After consuming the diets for 17 days, the rats were tested for audiogenic seizures and blood was then drawn for serum mineral analyses. Rats fed Mg-Ca = P =, Mg-Ca = P-, Mg-Ca+P = or Mg-Ca+P+ diets had high incidences of seizures. Those fed Mg-Ca-P =, Mg-Ca-P-, Mg-Ca = P+, Mg-Ca-P+ or Mg-Ca+P- diets had low incidences of seizures. In general, animals with low serum magnesium and calcium levels and high serum potassium levels were susceptible to audiogenic seizures. In this model, serum magnesium level is the most important determinant of seizure susceptibility, followed by calcium and potassium.

Acoustic Stimulation↗
PubMed1998

Magnesium deficiency in adult rats promotes the induction of ventricular tachycardia by the administration of epinephrine.

The effects of magnesium deficiency on epinephrine-induced ventricular tachyarrhythmia were investigated in adult rats. Forty-two adult Wistar rats were fed a magnesium-deficient diet while 30 rats were fed a standard diet for 20 days. The plasma magnesium concentration was lower in the magnesium-deficient rats (0.22+/-0.01 mmol/l) than in the control rats (0.76+/-0.03 mmol/l, P < 0.001). Using a telemetry system, electrocardiograms and arterial blood pressure were recorded on a polygraph in an unrestrained condition. Epinephrine was infused intravenously starting at 5 microg/kg per minute. The QT interval was prolonged to 50+/-1 ms in the magnesium-deficient rats compared with 44+/-1 ms in the control rats (P < 0.001). Before the administration of epinephrine, no ventricular tachyarrhythmias or seizures were found in either the control or the magnesium-deficient rats. The incidence of epinephrine-induced sustained ventricular tachycardia (VT) was higher in the magnesium-deficient rats (86%) than in the control rats (43%, P < 0.01). However, this VT did not result in sudden death. Seizures always preceded death in both the magnesium-deficient and control rats while the arrhythmias observed immediately before death were mainly bradyarrhythmias. The present study in an adult rat magnesium-deficient model revealed that magnesium deficiency enhances the susceptibility to epinephrine-induced ventricular tachyarrhythmias.

Animals↗
PubMed1980

Effect of magnesium deficiency on erythrocyte aging in rats.

Rats placed on a magnesium-deficient diet show decreased erythrocyte magnesium concentration, shortened erythrocyte survival, and erythrocyte membrane ultrastructure defects and become progressively anemic. Whether these pathologic processes are due to abnormal erythropoiesis or occur in the peripheral circulation is unknown. In the present study, magnesium and hemoglobin concentrations, reticulocyte count, erythrocyte pyrophosphatase, and pyruvate kinase activities were determined at weekly intervals for 6 weeks in whole blood and age-dependent erythrocyte fractions isolated from inbred Fisher rats fed a diet deficient in magnesium or the same diet with added magnesium. Freeze-fracture electron microscopic examinations were performed on age-dependent erythrocyte fractions to evaluate the membrane defect. The youngest red cells from magnesium-deficient rats were similar to those of control animals with respect to erythrocyte magnesium concentrations, pyrophosphatase activities, and membrane morphology. The older erythrocyte fractions from magnesium-deficient rats showed significant decreases in magnesium concentrations, pyrophosphatase activity, and the presence of membrane abnormalities. Thus, new erythrocytes produced in magnesium-deficient rats appear to be normal but rapidly develop biochemical and morphologic abnormalities with aging in a magnesium-deficient plasma environment.

Animals↗
PubMed1982

Hepatic gluconeogenic enzymes, plasma insulin and glucagon response to magnesium deficiency and fasting.

Three experiments were conducted to assess the effects of magnesium deficiency on the activities of hepatic glucose-6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FDPase) and phosphoenolpyruvate carboxykinase (PEPCK). Experiment 1 was designed to determine if magnesium deficiency interfered with the gluconeogenic response to fasting. Rats were fed either a control (C) or magnesium-deficient (MD) diet for 12 days. One-half of each group of rats was fasted for 24 hours prior to death. Hepatic enzyme activities, plasma and liver magnesium, and whole blood glucose were measured. Activities of G6Pase and PEPCK were higher in fasted group C rats compared to fed group C rats. Activity of FDPase was lower. The response was similar in the MD groups. Comparison of C and MD groups indicated that magnesium deficiency was accompanied by an increase in PEPCK activity. To verify this result and to investigate the role of anorexia in producing increased PEPCK activity, experiment 2 included a pair-fed group (PF). The results indicated that anorexia was not responsible for increased PEPCK activity in MD rats. The relation of circulating insulin and glucagon concentrations to effects of magnesium deficiency was explored in experiment 3. A decreased insulin:glucagon ratio was observed in MD rats. The results of these experiments suggest that magnesium deficiency alters PEPCK activity by affecting secretion of pancreatic hormones.

Animals↗
PubMed1997

Magnesium deficiency increases vasoconstrictor activity without affecting blood pressure of aged spontaneously hypertensive rats.

This study examines the effect of long-term magnesium-deficient diet on blood pressure and vascular reactivity in aged spontaneously hypertensive rats (SHR) with established hypertension. Thirty-one-week old male SHR received control (0.15 per cent magnesium) and magnesium-deficient (0.015 per cent magnesium) diets for 30 weeks. Systolic blood pressure was measured by tail-cuff method. At the end of the study, the heart, aorta and kidney were collected to measure total magnesium and calcium concentrations; the ex vivo effects of the different magnesium diets on vascular reactivity were examined in isolated aorta and in the isolated perfused mesenteric vascular bed. After 30 weeks, magnesium deficiency had no effect on systolic blood pressure and heart rate of SHR. The tissue concentrations of total magnesium in aorta, heart and kidney were not modified by magnesium deficient diet. Total calcium concentration was significantly higher in the heart of the SHR fed the magnesium-deficient diet (p < 0.01). The aortic responsiveness to contractile agents norepinephrine, endothelin-1, CaCl2 and KCl, and to vasorelaxant agents acetylcholine and isoproterenol were not modified by magnesium deficiency. The vasoconstrictor activity to norepinephrine, CaCl2 and KCl was significantly enhanced in the isolated perfused mesenteric vascular bed of magnesium-deficient SHR (p < 0.05). In conclusion, magnesium deficient diet fails to elevate blood pressure in aged SHR maintained on deficiency for 30 weeks despite an enhanced ex vivo vasoconstrictor activity.

Aging↗
PubMed1984

Reduction of plasma lecithin--cholesterol acyltransferase activity by acute magnesium deficiency in the rat.

Weanling Wistar rats were pair-fed for 8 days control and magnesium-deficient diets. Acute magnesium deficiency increased plasma triglycerides and free cholesterol levels and decreased esterified cholesterol levels. The plasma activity of lecithin--cholesterol acyltransferase was markedly diminished in fasting magnesium-deficient rats (54% reduction) and plasma high density lipoprotein (HDL) free cholesterol was significantly increased in the HDL fraction. The results of this study showing that dietary magnesium affects the activity of the enzyme involved in the esterification of free cholesterol to cholesterol ester provide a possible basis for the reduced plasma cholesterol esterification and hyperlipidemia associated with acute magnesium deficiency.

Animals↗
PubMed1981

Effect of magnesium deficiency on lipid metabolism in rats fed a high carbohydrate diet.

The effects of acute magnesium deficiency on lipid metabolism were examined in weaning rats fed a high carbohydrate diet containing starch or sucrose for 8 days. Rats were killed after the feeding period. In plasma, magnesium deficiency increased triglyceride and free cholesterol levels and decreased esterified cholesterol levels. Rats fed a magnesium-deficient diet containing sucrose showed particularly high triglyceride plasma levels. In liver, magnesium-deficient rats fed sucrose showed a significant increase in triglycerides, lactate and alpha-glycerophosphate and a significant decrease in glycogen. Changes in triglycerides and glycogen in the liver of magnesium-deficient rats fed starch were not significant. In sucrose-fed rats, serum lipoproteins were isolated by ultracentrifugation. With magnesium deficiency, triglycerides were significantly increased in the very low density lipoprotein (VLDL) and low density lipoprotein (LDL) fractions and cholesterol levels were increased in the VLDL and LDL and significantly lower in the high density lipoprotein (HDL) fractions. The detrimental effect of severe magnesium deficiency associated particularly with a high carbohydrate diet content and more especially with a sucrose diet is discussed.

Animals↗
PubMed1988

Enhanced vasoconstrictor responses to potassium, 5-hydroxytryptamine, and prostaglandin F2 alpha of isolated coronary arteries from magnesium-deficient rats. Comparison with vasomotor activity of aorta.

Wistar rats were fed a low magnesium diet for 8 or 12 weeks, resulting in reduced levels of magnesium in plasma, heart, and skeletal muscle, as compared with pair-fed control rats. The magnesium-deficient rats also had reduced tissue levels of potassium. Coronary arteries and thoracic aorta from magnesium-deficient rats and control rats were incubated in tissue baths and the contractile responses to potassium, 5-hydroxy-tryptamine, and prostaglandin F2 alpha were investigated using a sensitive in vitro system. The concentration-contraction curve, for all agents was shifted to the left in coronary arteries from magnesium-deficient rats. In aorta from magnesium-deficient rats, the pattern of change in reactivity to these agonists was not uniform: the concentration-contraction curve for 5-hydroxytryptamine was shifted to the left, the contractile response to prostaglandin F2 alpha was reduced, while there was no change in the response to potassium. The contractile response to the administration of calcium to calcium-depleted, potassium-depolarized vessels from magnesium-deficient rats was enhanced; the effect was more pronounced in coronary arteries as compared to the aorta. Hence, the vasomotor reactivity of coronary arteries appears to be more sensitive than is the aorta during magnesium-deficient conditions.

Animals↗
PubMed1996

Severe dietary magnesium deficiency does not alter levels and function of myocardial Gs alpha and Gi alpha.

Magnesium ions (Mg2+) play a crucial role in the activation and synthesis of guanine nucleotide-binding proteins (G proteins). However, there is no information about the influence of in vivo magnesium deficiency on the function and levels of G proteins. This study was done to investigate whether dietary magnesium deficiency alters function and levels of the two major myocardial G proteins, Gi alpha and Gs alpha. Severe hypomagnesemia and a significant reduction of myocardial magnesium occurred in rats fed a magnesium-deficient diet for 6 wk vs. rats fed a normal-magnesium diet (control). The magnesium-deficient rats developed focal myocardial lesions but their cardiac function was not impaired. Myocardial immunodetectable Gs alpha and Gi alpha levels of magnesium-deficient rats did not differ from control (Gs alpha: 2.39 +/- 0.52 vs. 2.76 +/- 0.72 arbitrary units/microgram protein, P > 0.05; Gi alpha: 1.60 +/- 0.52 vs. 1.89 +/- 0.30 arbitrary units/microgram protein, P > 0.05). Similarly, the function of Gs alpha and Gi alpha estimated by basal and ligand-stimulated adenylyl cyclase activity was not significantly different between the two groups of animals. The results show that dietary-derived magnesium deficiency sufficient to produce severe hypomagnesemia does not produce any significant change in levels or function of myocardial G proteins.

Adenylyl Cyclases↗
PubMed1995

Triglyceride-rich lipoproteins from magnesium-deficient rats are more susceptible to oxidation by cells and promote proliferation of cultured vascular smooth muscle cells.

An important characteristic of hyperlipaemia associated with magnesium deficiency in rats is the postprandial accumulation of triglyceride-rich lipoproteins (TGRLP). The present investigation was performed to determine the susceptibility of TGRLP isolated from magnesium-deficient rats to metal ion and cell dependent peroxidation and the effect of these lipoproteins on cultured vascular smooth muscle cells (VSMC). TGRLP were isolated by sequential ultracentrifugation from plasma of control and magnesium-deficient rats fed for 8 d on adequate or magnesium-deficient diets. Magnesium-deficient animals were hypertriglyceridemic as compared to control rats. After exposure to oxidative stress in vitro, Cu2+ or activated macrophages, conjugated diene production was significantly higher in TGRLP isolated from magnesium-deficient rats. Culture of VSMC with TGRLP from magnesium-deficient rats resulted in more important cell growth than with lipoproteins isolated from control animals. After incubation with VSMC, TGRLP from magnesium-deficient rats showed higher conjugated diene production than those from control rats. These results support the atherogenic properties of magnesium deficiency, which is accompanied by hyperlipaemia and which affects two important linked pathways in atherosclerosis, lipoprotein peroxidation and VSMC proliferation.

Animals↗
PubMed2005

Magnesium deficiency is associated with insulin resistance in obese children.

OBJECTIVE: Magnesium deficiency has been associated with insulin resistance (IR) and increased risk for type 2 diabetes in adults. This study was designed to determine whether obese children exhibit serum or dietary magnesium deficiency and its potential association with IR. RESEARCH DESIGN AND METHODS: We studied 24 obese nondiabetic children (BMI > or =85th percentile) and 24 sex- and puberty-matched lean control subjects (BMI <85th percentile). We measured serum magnesium, indexes of insulin sensitivity, dietary magnesium intake (using a food frequency questionnaire), and body composition (by air displacement plethysmography). RESULTS: Serum magnesium was significantly lower in obese children (0.748 +/- 0.015 mmol/l, means +/- SE) compared with lean children (0.801 +/- 0.012 mmol/l) (P = 0.009). Serum magnesium was inversely correlated with fasting insulin (r(s) = -0.36 [95% CI -0.59 to -0.08]; P = 0.011) and positively correlated with quantitative insulin sensitivity check index (QUICKI) (0.35 [0.06-0.58]; P = 0.015). Dietary magnesium intake was significantly lower in obese children (obese: 0.12 +/- 0.004 vs. lean: 0.14 +/- 0.004 mg/kcal; P = 0.003). Dietary magnesium intake was inversely associated with fasting insulin (-0.43 [-0.64 to -0.16]; P = 0.002) and directly correlated with QUICKI (0.43 [0.16-0.64]; P = 0.002). CONCLUSIONS: The association between magnesium deficiency and IR is present during childhood. Serum magnesium deficiency in obese children may be secondary to decreased dietary magnesium intake. Magnesium supplementation or increased intake of magnesium-rich foods may be an important tool in the prevention of type 2 diabetes in obese children.

Adipose Tissue↗
PubMed1997

Quinolone-induced arthropathy: exposure of magnesium-deficient aged rats or immature rats, mineral concentrations in target tissues and pharmacokinetics.

Quinolone treatment or magnesium deficiency induce identical cartilage lesions in juvenile rats and show additive arthropathogenic effects. It has been shown previously that neither condition is arthropathogenic in 8-week-old rats. Joint cartilage from aged individuals is rather prone to pathological alterations but information on prolonged quinolone treatment and/or dietarily induced magnesium deficiency in aged animals is not available. We treated magnesium-deficient (n = 9) aged Wistar rats (age 15 months) and age-matched controls with daily doses of 600 mg ofloxacin/kg body wt. by gastric intubation for 28 days. Further groups of magnesium-deficient and control rats (n = 9 and n = 10, respectively) received the vehicle only. Peak plasma concentrations of ofloxacin in adult rats were 20.5 +/- 5.6 mg/l (mean +/- SD) following treatment with a single dose of 600 mg/kg body wt. At the end of the experiment the degree of magnesium deficiency was most pronounced in plasma (Mg2+-def., 0.33 +/- 0.12 mmol/l; control, 0.97 +/- 0.08 mmol/l) and less pronounced in sternal cartilage (Mg2+-def., 10.8 +/- 3.6 mmol/kg dry wt; control, 13.3 +/- 2.8 mmol/kg dry wt), whereas the magnesium concentration in femoral bone remained unchanged (Mg2+-def., 201 +/- 13 mmol/kg dry wt; control, 204 +/- 11 mmol/kg dry wt). Histological investigation of the knee joints revealed no cartilage lesions following ofloxacin treatment, magnesium deficiency or a combination of both conditions. By contrast, cartilage lesions such as scars and erosions of the joint surface, chondrocyte clusters within acellular areas of the cartilage matrix and persisting clefts were detectable in knee joints from 7 of 10 adult rats (age 9 months) which had been treated with 4 x 600 mg fleroxacin/kg body wt. at 5 weeks of age. Mean plasma concentration of fleroxacin in juvenile rats was approx. 50 mg/l between 1.5 and 6 h after dosing and the drug was still detectable in plasma 48 h after dosing (0.4 +/- 0.1 mg/l). Our data indicate that joint cartilage in aged rats is not altered by a 4-week quinolone treatment, even during magnesium deficiency. Cartilage lesions in adult rats were only detectable if the animals had been treated during the sensitive phase at 5 weeks postnatally.

Age Factors↗
PubMed1983

Influence of maternal magnesium deficiency on tissue lead content of rats.

Diets containing 150 or 600 ppm magnesium with or without 200 ppm lead were fed to rats throughout gestation and lactation to determine the influence of moderate magnesium deficiency on tissue lead content of maternal and offspring tissue. During lactation it was necessary to increase the lowest dietary magnesium level to 225 ppm. Lead caused a significant depression in both gestational weight gain and average pup weight regardless of the level of dietary magnesium. Maternal magnesium deficiency was evidenced by significant reductions in serum and tibia magnesium, a 17-fold increase in kidney calcium, and hyperemia of the ears. In offspring, however, only growth and tibia magnesium were significantly affected by the magnesium deficiency, and the maternal-fetal difference in serum and tibia magnesium concentration was maintained. Maternal magnesium deficiency resulted in significantly higher lead concentrations in dam liver, and offspring erythrocytes, liver and tibia. A mechanism for the enhanced accumulation of lead in maternal and offspring tissue as a result of maternal magnesium deficiency is not defined, but it is likely to involve enhanced intestinal lead absorption.

Animals↗
PubMed1975

Protective effect of coexistent thiamine deficiency upon the experimental cardiomyopathy associated with acute magnesium deficiency in the Syrian golden hamster.

Repeated efforts to induce beriberi heart disease by experimental thiamine deficiency (B1d) have failed in many species. To test the hypothesis that magnesium deficiency (Mgd) might be the cofactor necessary for heart failure, 10-week-old Syrian golden hamsters were divided into four groups-control (C), B1d, Mgd, and combined MgB1d-and were fed the diets ad libitum for 3 weeks. On day 21, animals were studied under intraperitoneal pentobarbital anesthesia (50 mg/kg). Electrocardiograms were taken and right and left ventricular pressures were measured by transthoracic needle puncture. Cardiac output was measured by the direct Fick method. The complete study was performed in 9 C, 13 B1d, 9 Mgd, and 14 MgB1d animals. B1d was proven by low red blood cell transketolate high B1 pyrophosphate effect, and was accompanied by tachycardia and hypercalcemia. B1 did not differ from C in any other parameter. Mgd was characterized by hypomagnesemia, hypercalcemia, prolongation of the PR interval, widening of the QRS interval, low O2 consumption, low cardiac output, and increased heart weight to body weight ratio (HW/BW) as compared to control. No differences were observed in right and left ventricular pressures or peak /dt. MgB1d was characterized by hypomagnesium, hypercalcemia, low red blood cell transkeotlase, and high B1 pyrophosphate effect. MgB1d minimized the deleterious effects of Mgd: animals were more active and the mortality was low, the PR interval remained normal, the QRS interval widened significantly less, cardiac output remained normal, and HW/BW increased significantly less. Although, once again, beriberi heart disease was not produced, B1d appeared to exert a protective effect upon the Mg-deficient myocardium.

Acute Disease↗
PubMed2000

Effects of magnesium deficiency on joint cartilage in immature beagle dogs: immunohistochemistry, electron microscopy, and mineral concentrations.

Quinolone-induced chondrotoxicity is possibly associated with the magnesium-chelating properties of quinolones. This toxic effect seems to be restricted to a rather short time period during postnatal development as shown in rats and dogs. We studied developmental changes of the integrin pattern on canine chondrocytes (e.g. the alpha(v)beta(3)- or alpha(5)beta(1)-integrin), because integrin function depends on divalent cations, as well as the matrix composition (e.g., collagen type II, fibronectin), in 11-, 18-, and 55-week-old Beagles (n=8) by immunohistochemistry. We also analyzed the magnesium and calcium content by atomic absorption spectroscopy in cartilage and bone and studied the effects of a magnesium-deficient diet on joint cartilage in four immature Beagles (18 weeks old at necropsy). The dogs were fed the magnesium-deficient diet for 40 to 46 days. All dogs exhibited gait alterations ('limping') after 4 weeks on the magnesium-deficient diet. Male, magnesium-deficient dogs exhibited pronounced weakness in their front legs; in one of these dogs the front legs were hyperextended to a 90 degrees angle. We observed no significant differences in the integrin pattern in samples from dogs at different developmental stages or in magnesium-deficient dogs in comparison to age-matched controls. Localization of fibronectin in the joint cartilage was found to vary with the age of the dogs as well as with the site of collection. In the middle zone of immature joint cartilage, corresponding to the predilective site of quinolone-induced cartilage lesions, we observed a slight increase in staining with the fibronectin antibody in some samples from magnesium-deficient dogs. Electron microscopy revealed alterations in chondrocytes from the magnesium-deficient dogs (e.g., swollen mitochondria and enlarged endoplasmic reticulum) which are also seen after treatment with quinolones. In summary, we found no significant differences of the integrin pattern on chondrocytes from joint cartilage of dogs at various developmental stages. However, magnesium deficiency in immature dogs induced similar clinical symptoms as quinolone treatment as well as distinct alterations in chondrocytic fibronectin staining and their ultrastructure. This corroborates our findings in rats where magnesium chelation is an important event in quinolone-induced chondrotoxicity.

Animals↗
PubMed2000

Magnesium deficiency in patients with chronic pancreatitis identified by an intravenous loading test.

Magnesium deficiency is a common clinical condition that may exist despite a normal serum magnesium concentration. Patients with chronic pancreatitis could develop magnesium deficiency due to either malabsorption, diabetes mellitus, or chronic alcoholism. Since serum levels of magnesium are a poor indicator of magnesium deficiency, the retention of a low-dose intravenous magnesium load (0.1 mmol/kg body weight) was determined in 13 patients with chronic pancreatitis (10 due to alcoholism) and eight healthy controls. Percentage magnesium retention was greater in patients with chronic pancreatitis than controls (59.8+/-37.3% S.D. versus 22.0+/-38.2% S. D.: P=0.038), and 10 of 13 patients showed evidence of magnesium deficiency. Routine evaluation of magnesium status could allow appropriate supplementation and conceivably symptomatic improvement in patients with severe chronic pancreatitis.

Adult↗
PubMed1975

Mast cell increase in the duodenum and kidney of magnesium-deficient rats.

Rats were maintained on a magnesium-deficient diet for 1 to 5 weeks to study the mast cell (MC) populations in their duodenum and kidney. A marked increase of intestinal subepithelial mast cells was observed in these animals as compared with normal controls. The cells in both groups showed an identical reaction for mucopolysaccharides but the 5-hydroxytryptamine content tended to be higher in the cells of magnesium-deficient animals. Proliferation of MC was also observed in the renal cortex of the magnesium-deficient rats. This finding is significant because MC are known to be virtually absent from normal kidneys. Magnesium deprivation resulted in numerous MC not only in the intertubular spaces but also within the glomeruli. Possible correlations between these and other pertinent observations are discussed with regard to certain renal diseases. The discussion is extended to the possible mechanism through which magnesium could influence secretory processes in MC.

Alcian Blue↗
PubMed1994

Combined effects of magnesium deficiency and an atherogenic level of low density lipoprotein on uptake and metabolism of low density lipoprotein by cultured human endothelial cells. II. Electron microscopic data.

The effects of magnesium deficiency on low density lipoprotein (LDL) transport by cultured endothelial cells with a high concentration of LDL (2 mg of LDL cholesterol/ml) were investigated by electron microscopy and by counting the radioactivity of [3H]-LDL transported across an endothelial monolayer grown on culture plate inserts. Electron microscopic examination showed that the number of pits/vesicles in the apical side was time-dependently increased for 24 h in both magnesium-deficient and magnesium-sufficient groups with the exception of 1 h under magnesium sufficiency. The number of pits/vesicles in the basal side was also increased for 8 h in both groups, though there was a decrease at 24 h in the two groups. No difference between either magnesium group at the same time point was statistically significant. [3H]-LDL transport was also time-dependently increased in both magnesium-deficient and magnesium-sufficient groups. In contrast to the results obtained by electron microscopy, the amount of LDL transported under magnesium deficiency was much larger for 24 h than under magnesium sufficiency. Differences in LDL transport between magnesium groups were statistically significant at 4 and 8 h. This finding indicates that magnesium deficiency increases LDL transport across the endothelial monolayer. The increase may be due to energy-dependent movement across endothelial cells, energy-independent movement between cells, or both. However, we conclude that magnesium deficiency increases the energy-dependent LDL transport to some degree since intercellular gap formations were rarely observed in either magnesium group. This LDL transported to the subendothelial space may lead to LDL accumulation and initiate atherosclerosis.

Arteriosclerosis↗