John Libbey Eurotext

Magnesium Research

Failure of β-cell function for compensate variation in insulin sensitivity in hypomagnesemic subjects Volume 22, numéro 3, september 2009


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To evaluate if decreased insulin sensitivity is appropriately compensated by β-cell function in subjects with hypomagnesemia, 165 individuals, 20 to 65 years of age, were randomly enrolled in a cross-sectional study. Subjects were allocated into groups with and without hypomagnesemia, matched by age, gender, waist circumference, and body mass index. Pregnancy, smoking, alcohol consumption, high blood pressure, type 2 diabetes, chronic diarrhea, renal disease, malignancy, and heavy physical activity were exclusion criteria. Hypomagnesemia was defined by a serum magnesium concentration of < 1.8 mg/dL. As a surrogate of the hyperbolic model of β-cell function, the relation between Belfiore’s index {2/[1 + (Fasting insulin pmol/L x Fasting glucose mmol/L)]} and the HOMA-β index {20 X Fasting insulin μU/mL /(Fasting glucose mmol/L – 3.5)} was used. The mean Area Under Curve (AUC) was calculated for each group. Although the Belfiore index was significantly lower (0.041 ± 0.021 and 0.053 ± 0.030, p = 0.005) and fasting plasma glucose higher (113.6 ± 23.0 and 106.8 ± 18.4 mg/dL, p = 0.04) in the subjects with hypomagnesemia, the HOMA-β index (82.5 ± 48.5 and 91.2 ± 79.9, p = 0.32) and insulin levels (8.6 ± 5.4 and 9.6 ± 4.8 μU/mL, p = 0.17) were similar between the groups studied. The AUC which evaluates the adaptation of beta-cell function to variation in insulin sensitivity was significantly higher in the normomagnesemic than the hypomagnesemic group (proportion 1:2.5). Results of this study show that the decrease in insulin sensitivity is not appropriately compensated by β-cell function in individuals with hypomagnesemia; our finding suggests that hypomagnesemia could be linked to inadequate β-cell compensation.