Serum and urinary magnesium in young diabetic subjects in Bangladesh

Citation
La. Khan et al., Serum and urinary magnesium in young diabetic subjects in Bangladesh, AM J CLIN N, 69(1), 1999, pp. 70-73
Citations number
21
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF CLINICAL NUTRITION
ISSN journal
00029165 → ACNP
Volume
69
Issue
1
Year of publication
1999
Pages
70 - 73
Database
ISI
SICI code
0002-9165(199901)69:1<70:SAUMIY>2.0.ZU;2-I
Abstract
Background: Magnesium imbalance, implicated in diabetes mellitus both as a cause and a consequence, has not yet been investigated in subgroups of subj ects with malnutrition-related diabetes mellitus, which is prevalent in you ng patients in tropical developing countries such as Bangladesh. Objective: The present study evaluated the serum and urinary magnesium conc entrations 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 alone with 13 healthy contr ol and 13 malnourished control subjects [body mass index (in kg/m(2)) <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, respectiv ely) 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 heal thy and malnourished control subjects, respectively) concentration. Subject s 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 bot h control groups. In contrast with 0% of healthy and 7.7% of malnourished c ontrol subjects, 42.85% of type 2 diabetic subjects, 61.54% of those with P DDM. and 69.23% of those with FCPD were hypomagnesemic, Subjects with FCPD and PDDM had significantly higher urinary excretion of magnesium than the h ealthy 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 caus e of diabetes mellitus.