February 01, 2016
1 min read

Vitamin D fails to improve glucose homeostasis in prediabetes, type 2 diabetes

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In patients with prediabetes or diet-treated type 2 diabetes, an 8-week regimen of high-dose vitamin D does not appear to confer any significant benefits to beta-cell function, insulin sensitivity or glycemic control, according to recent findings.

Henrik Wagner, a PhD student at Karolinska Institutet in Sweden, and colleagues evaluated 44 patients with prediabetes or diet-treated type 2 diabetes recruited from the Stockholm Diabetes Prevention Program to determine the effect of high-dose vitamin D3 treatment on beta-cell function, insulin sensitivity and glucose tolerance.

Participants were randomly assigned to one of two treatment groups: vitamin D3 30,000 IU administered orally once a week (n = 21) or matching placebo oil (n = 22). Initial dosing was given at the randomization visit, the fifth dose was administered at the half-time assessment and the participants took the remaining six doses at home.

Researchers found that, in the intervention group, season-adjusted concentration of 25-hydroxyvitamin D levels were double, whereas no change was found in the placebo group. Regarding the primary endpoint of first-phase insulin secretion, a tendency to increase was observed in the intervention group, and a significant increase was found in the placebo group; no difference was found between the two groups. Moreover, no changes in second-phase insulin secretion or insulin sensitivity were found within or between the two groups. Both groups demonstrated an increase in first-phase disposition index; no difference was found between the two groups. In the intervention group, second-phase disposition index showed a tendency to increase, but no significant different toward placebo was found.

“According to the findings of our study, we see no implication for vitamin D treatment to affect glucose homeostasis in subjects with abnormal glucose tolerance,” the researchers wrote. – by Jennifer Byrne

Disclosure: The study was funded in part by Merck and Renapharma AB. The researchers report no relevant financial disclosures.