Objective: A positive correlation between levels of 25-hydroxyvitamin D [25(OH)D] and insulin sensitivity has been shown in healthy subjects. We aimed to test the hypothesis that concentration of 25(OH)D influences insulin sensitivity in obesity before and after weight loss.
Research methods and procedures: We investigated the relation between serum 25(OH)D and insulin sensitivity (estimated by euglycemic-hyperinsulinemic clamp) in 116 obese women (BMI > or = 40 kg/m2) evaluated before and 5 and 10 years after biliopancreatic diversion (BPD). Body composition was estimated by the isotope dilution method.
Results: Prevalence of hypovitaminosis D was 76% in the obese status and 91% and 89% at 5 and 10 years after BPD, respectively, despite ergocalciferol supplementation. 25(OH)D concentration decreased from 39.2 +/- 22.3 in obesity (p = 0.0001) to 27.4 +/- 16.4 and 25.1 +/- 13.9 nM 5 and 10 years after BPD, respectively. Whole-body glucose uptake increased from 24.27 +/- 4.44 at the baseline to 57.29 +/- 11.56 and 57.71 +/- 8.41 mumol/kg(fat free mass) per minute 5 and 10 years after BPD, respectively (p = 0.0001). Predictor of 25(OH)D was fat mass (R2 = 0.26, p = 0.0001 in obesity; R2 = 0.20, p = 0.02 after BPD). Parathormone correlated with fat mass (R2 = 0.19; p = 0.0001) and BMI (R2 = 0.053; p = 0.01) and inversely with M value (R2 = 0.16; p = 0.0001), but only in obese subjects.
Discussion: A high prevalence of hypovitaminosis D was observed in morbid obesity both before and after BPD. Low 25(OH)D did not necessarily imply increased insulin resistance after BPD, a condition where, probably, more powerful determinants of insulin sensitivity overcome the low circulating 25(OH)D levels. However, the present data cannot exclude some kind of influence of vitamin D status on glucose and insulin metabolism.