Serum and urinary magnesium in young diabetic subjects in Bangladesh

Abstract

Background: 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. Objective: The present study evaluated the serum and urinary magnesium concentrations in groups of young diabetic subjects in Bangladesh. Design: 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. Results: 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. Conclusions: 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.