Mechanism of increased erythrocyte membrane fluidity during magnesium deficiency in weanling rats

Abstract

The erythrocyte membrane was investigated in weanling male rats pair fed with magnesium-deficient and control diets for 8 days. Fluorescence polarization studies revealed a 15% increase in the fluidity of membranes from deficient rats. A similar increase in the fluidity of liposomes indicated that protein was not involved. The change was associated with decreased osmotic fragility of intact erythrocytes; the cells lost their biconcavity and had a flattened appearance with surface irregularities. Analysis of the membranes showed decreased amounts of magnesium, cholesterol, and sphingomyelin in the deficient group. The reduced ratios of cholesterol to phospholipid and sphingomyelin to phosphatidylcholine were consistent with the increased fluidity. Addition of physiological amounts of magnesium to the medium rigidified membranes incubated in tris(hydroxymethyl)-aminomethane buffer, and this was prevented by the presence of EDTA. Cross-incubation experiments with erythrocyte ghosts and plasma from the two groups of rats showed that magnesium-deficient plasma increased the fluidity of control ghosts and control plasma rigidified ghosts from magnesium-deficient rats. Addition of sufficient magnesium chloride to raise the magnesium content of deficient plasma to normal had no significant effect. These results show that the increased fluidity of the erythrocyte membrane in magnesium deficiency is due to physicochemical exchange with the plasma. Although magnesium can directly influence membrane fluidity, the change during its deficiency in vivo is mainly mediated indirectly via disturbances in lipid metabolism.

Magnesium Deficiency in Type 2 Diabetes

“…First of all, it is an essential cofactor in reactions involving phosphorylation; thus, magnesium de fi ciency could impair the insulin signal transduction pathway [ 46,47 ] . Second, low serum or erythrocyte magnesium levels may affect the interaction between insulin and insulin receptor by decreasing hormone receptor af fi nity or by increasing membrane microviscosity [ 48 ] . Finally, magnesium can also be a limiting factor in carbohydrate metabolism, since many of the enzymes in this process require magnesium as a cofactor during reactions that utilize phosphorus bond [ 49,50 ] .…”

Implications of Magnesium Deficiency in Type 2 Diabetes: A Review

“…First of all, it is an essential cofactor in reactions involving phosphorylation; thus, magnesium deficiency could impair the insulin signal transduction pathway [63,64]. Second, low serum or erythrocyte magnesium levels may affect the interaction between insulin and insulin receptor by decreasing hormone receptor affinity or by increasing membrane microviscosity [65]. Finally, magnesium can also be a limiting factor in carbohydrate metabolism since many of the enzymes in this process require magnesium as a cofactor during reactions that utilize phosphorus bond [66][67][68].…”

Magnesium Deficiency Is Associated With Insulin Resistance in Obese Children

“…Magnesium deficiency is associated with increased intracellular calcium levels, which may lead to IR (20). Low erythrocyte magnesium content increases membrane microviscosity, which may impair insulin interaction with its receptor (21). Tyrosine kinase activity is decreased in muscle insulin receptors of rats fed a low-magnesium diet (22).…”