Abstract
Vitamin D (D₃) status is reported to correlate negatively with insulin production and insulin sensitivity in patients with type 2 diabetes mellitus (T2DM). However, few placebo-controlled intervention data are available. We aimed to assess the effect of large doses of parenteral D3 on glycosylated haemoglobin (HbA(₁c)) and estimates of insulin action (homeostasis model assessment insulin resistance: HOMA-IR) in patients with stable T2DM. We performed a prospective, randomised, double-blind, placebo-controlled pilot study at a single university care setting in Switzerland. Fifty-five patients of both genders with T2DM of more than 10 years were enrolled and randomised to either 300,000 IU D₃ or placebo, intramuscularly. The primary endpoint was the intergroup difference in HbA(₁c) levels. Secondary endpoints were: changes in insulin sensitivity, albuminuria, calcium/phosphate metabolism, activity of the renin-aldosterone axis and changes in 24-hour ambulatory blood pressure values. After 6 months of D₃ supply, there was a significant intergroup difference in the change in HbA(₁c) levels (relative change [mean ± standard deviation] +2.9% ± 1.5% in the D₃ group vs +6.9% ± 2.1% the in placebo group, p = 0.041) as HOMA-IR decreased by 12.8% ± 5.6% in the D₃ group and increased by 10% ± 5.4% in the placebo group (intergroup difference, p = 0.032). Twenty-four-hour urinary albumin excretion decreased in the D₃ group from 200 ± 41 to 126 ± 39, p = 0.021). There was no significant intergroup difference for the other secondary endpoints. D₃ improved insulin sensitivity (based on HOMA-IR) and affected the course of HbA(₁c) positively compared with placebo in patients with T2DM.
Highlights
Epidemiological and observational evidence suggests that vitamin D (D3) supply inversely correlates with the risk for type 2 diabetes mellitus (T2DM) and, once diabetic, serum 25(OH)-D3 levels correlate inversely with impaired glucose tolerance [1, 2]
We aimed to assess the effect of large doses of parenteral D3 on glycosylated haemoglobin (HbA1c) and estimates of insulin action in patients with stable T2DM
After 6 months of D3 supply, there was a significant intergroup difference in the change in HbA1c levels as homeostasis model assessment Homeostasis model assessment insulin resistance (HOMA-IR) (HOMA)-IR decreased by 12.8% ±
Summary
Epidemiological and observational evidence suggests that vitamin D (D3) supply inversely correlates with the risk for T2DM and, once diabetic, serum 25(OH)-D3 levels correlate inversely with impaired glucose tolerance [1, 2]. D3 is required for and improves the production of insulin, and is implicated in the mechanism of insulin action [3, 4] In both nondiabetic and diabetic patients, the clinical associations of D3 with insulin resistance and beta-cell function are inconsistent [2, 5, 6], and reported intervention studies employing D3 either as 25(OH)-D3 (e.g., cholecalciferol) or as 1,25(OH)2-D3 (e.g., calcitriol) have yielded conflicting results that are difficult to interpret owing to lack of placebo control [7, 8]. In view of the suggestive but inconclusive evidence for a clinically important effect of exogenous D3 supplementation on glucose and insulin homeostasis in both normal and diabetic subjects and as few placebo-controlled intervention data are available, we wished to assess insulin sensitivity to large doses of D3 in a double-blinded, randomised, placebo-controlled trial in stable T2DM patients. In view of the lack of information on responses of calcium/phosphate metabolism, calci-/phosphotropic hormones and 24-hour ambulatory blood pressures to large doses of D3 in T2DM patients, this study explored these data
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