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

Biomedical Research Unit, Mexican Social Security Institute, Durango, Mexico, and The Research Group on Diabetes, Durango, Mexico
  • Mots-clés : beta-cell function, insulin sensitivity, magnesium
  • DOI : 10.1684/mrh.2009.0180
  • Page(s) : 151-6
  • Année de parution : 2009

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.