Serum and urinary magnesium in young diabetic subjects in Bangladesh

Magnesium imbalance, implicated in diabetes mellitus both as a cause and a consequence, has not yet been investigated in subgroups of subjects with malnutrition-related diabetes mellitus. which is prevalent in young patients in tropical developing countries such as Bangladesh.

The present study evaluated the serum and urinary magnesium concentrations in groups of young diabetic subjects in Bangladesh.

Forty patients newly diagnosed with diabetes [13 with fibrocalculus pancreatic diabetes (FCPD), 13 with protein-deficient diabetes (PDDM), and 14 with type 2 diabetes mellitus] were studied along with 13 healthy control and 13 malnourished control subjects [body mass index (in kg/m2) < 19]. Magnesium was measured by atomic absorption spectrophotometry.

Malnutrition itself was not related to the serum glucose (fasting: 3.68+/-0.74 and 4.11+/-0.29 mmol/L; postprandial: 6.30+/-0.41 and 6.00+/-0.24 mmol/L for healthy and malnourished control subjects, respectively) or serum or urinary magnesium (serum: 0.73+/-0.03 and 0.75+/-0.05 mmol/L: urinary: 232+/-124 and 243+/-88 mmol Mg/mol creatinine for healthy and malnourished control subjects, respectively) concentration. Subjects with FCPD and PDDM had significantly lower serum magnesium concentrations (PDDM: 0.68+/-0.06 mmol/L, FCPD: 0.66+/-0.07 mmol/L) than those in both control groups. In contrast with 0% of healthy and 7.7% of malnourished control subjects, 42.85% of type 2 diabetic subjects, 61.54% of those with PDDM, and 69.23% of those with FCPD were hypomagnesemic. Subjects with FCPD and PDDM had significantly higher urinary excretion of magnesium than the healthy and malnourished control subjects and the type 2 diabetic subjects. Hypermagnesuria paralleled hypomagnesemia.

Malnutrition may not itself give rise to glucose intolerance, and serum magnesium deficiency seems to be a consequence rather than a cause of diabetes mellitus.