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07-24-2019 | Type 2 diabetes | News

Vitamin D may slow type 2 diabetes progression


medwireNews: High-dose vitamin D supplementation may slow type 2 diabetes progression by increasing peripheral insulin sensitivity and beta cell function in people at high risk for or newly diagnosed with the condition, randomized trial data show.

In a statement to the press, lead researcher Claudia Gagnon, from Université Laval in Québec, Canada, said: “Type 2 diabetes and prediabetes are a growing public health concern and although our results are promising, further studies are required to confirm our findings, to identify whether some people may benefit more from this intervention, and to evaluate the safety of high-dose vitamin D supplementation in the long term.

“Until then I would suggest that current vitamin D supplementation recommendations be followed.”

Gagnon and team found that after 6 months of daily supplementation with vitamin D3 5000 IU, peripheral insulin sensitivity – measured according to the M-value derived from a 2-hour hyperinsulinemic-euglycemic clamp – increased by a mean 22.9% among the 48 participants randomly assigned to this treatment, from a baseline value of 3.97 mg/kg per min to a follow-up value of 4.88 mg/kg per min.

By contrast, there was no change in the M-value from baseline to 6 months (4.15 vs 4.12 mg/kg per min) among the 48 participants randomly assigned to receive placebo. This resulted in a significantly greater mean change with vitamin D relative to placebo (0.92 vs –0.03).

Furthermore, an exploratory post-hoc analysis revealed that between-group differences in M-value were only significant among participants with diabetes or prediabetes at baseline, but not among those with normal glucose tolerance who had other risk factors for diabetes such as an increased waist circumference, a fasting triglyceride level above 1.7 mM, or a history of gestational diabetes.

The researchers also found that the change in beta-cell function, as measured by the disposition index, was significantly greater in the vitamin D group than in the placebo group, with an average increase of 267.0 points in the former group versus a decrease of 55.5 points in the latter, from baseline levels of 2425.5 and 1768.1, respectively.

There was no effect, however, on other measures of insulin sensitivity (HOMA2%S, Matsuda index) or on insulin secretion (insulinogenic index, C-peptide area under the curve, HOMA2-B), oral glucose tolerance, glycated hemoglobin, and anthropometric measurements.

Writing in the European Journal of Endocrinology, Gagnon and co-authors suggest: “The discordant effects of vitamin D supplementation that we observed on insulin sensitivity measures, with a significant beneficial effect on M-value and no difference on HOMA2%S and Matsuda indices, [suggest] that vitamin D acts mainly on peripheral insulin sensitivity.

“Indeed, HOMA2%S primarily reflects hepatic insulin sensitivity, and Matsuda whole-body insulin sensitivity with a major contribution of hepatic insulin sensitivity whereas the hyperinsulinemic-euglycemic clamp (M-value), at the insulin dose that we used, evaluates predominantly muscle insulin sensitivity.”

In the press statement Gagnon also acknowledged that their findings differed from those of vitamin D trials among people with long-standing type 2 diabetes for whom no benefit was seen, but said the reasons for such differences are unclear.

She said: “This could be due to the fact that improvements in metabolic function are harder to detect in those with longer-term disease or that a longer treatment time is needed to see the benefits.”

Of note, the study by Gagnon et al was conducted before the publication of data from the D2d trial, which found that high-dose vitamin D did not significantly reduce the risk for developing type 2 diabetes among people with prediabetes, as reported by medwireNews.

By Laura Cowen

medwireNews is an independent medical news service provided by Springer Healthcare. © 2019 Springer Healthcare part of the Springer Nature group

Eur J Endocrinol 2019; doi:10.1530/EJE-19-0156


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