Diabetes not treated by single dose of vitamin D – RCT

Effects of Vitamin D Supplementation on Insulin Sensitivity and Insulin Secretion in Subjects With Type 2 Diabetes and Vitamin D Deficiency: A Randomized Controlled Trial

Diabetes Care 2017;40:872-878 | https://doi.org/10.2337/dc16-2302, accepted 11 April 2017

Hanne L. Gulseth,1,2 Cecilie Wium,1,2 Kristin Angel,3 Erik F. Eriksen,1,4 and Kare I. Birkeland1,4

1Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway

2Hormone Laboratory, Oslo University Hospital, Oslo, Norway

3Department of Cardiology, Oslo University Hospital, Oslo, Norway

4Institute of Clinical Medicine, University of Oslo, Oslo, Norway

Corresponding author: Hanne L. Gulseth, h.l.gulseth@medisin.uio.no.

Intervention group had < 40 ng by the end of the first month Need to have > 40 nanograms for many months to treat diabetes * Diabetes treated by vitamin D when levels exceeded 61 ng – Sept 2015 * Diabetes not prevented or treated if give only modest amount of vitamin D or for short period of time – meta-analysis July 2014 * Vitamin D injection is far better than oral for diabetics (poor gut) – RCT March 2017 Describes many low-cost gut-friendly forms of Vitamin D * Diabetes treated if given enough vitamin D (example: 50,000 IU weekly) – review of RCT - Jan 2017 1. Overview Diabetes and vitamin D contains the following summary {include} 1. Diabetes category starts with the following {include}

OBJECTIVE

In observational studies, low vitamin D levels are associated with type 2 diabetes (T2D), impaired glucose metabolism, insulin sensitivity, and insulin secretion. We evaluated the efficacy of vitamin D supplementation on insulin sensitivity and insulin secretion in subjects with T2D and low vitamin D (25-hydroxyvitamin D [25(OH) D] <50 nmol/L).

RESEARCH DESIGN AND METHODS

Sixty-two men and women with T2D and vitamin D deficiency participated in a 6-month randomized, double-blind, placebo-controlled trial. Participants received a single dose of 400,000 IU oral vitamin D3 or placebo, and the vitamin D group received an additional 200,000 IU D3 if serum 25(OH)D was <100 nmol/L after 4 weeks. Primary end points were total Rd by euglycemic clamp with assessment of endogenous glucose production and first-phase insulin secretion by intravenous glucose tolerance test.

RESULTS

In the vitamin D group, the mean ± SD baseline serum 25(OH)D of 38.0 ± 12.6 nmol/L increased to 96.9 ± 18.3 nmol/L after 4 weeks, 73.2 ± 13.7 nmol/L after 3 months, and 53.7 ± 9.2 nmol/L after 6 months. The total exposure to 25(OH)D during 6 months (area under the curve) was 1,870 ± 192 and 1,090 ± 377 nmol/L per week in the vitamin D and placebo groups, respectively (P < 0.001). Insulin sensitivity, endogenous glucose production, and glycemic control did not differ between or within groups after treatment (P = 0.52). First-phase insulin secretion did not change significantly after treatment (P = 0.10)

CONCLUSIONS

Replenishment with a large dose of vitamin D3 to patients with T2D and vitamin D deficiency did not change insulin sensitivity or insulin secretion. These findings do not support such use of therapeutic vitamin D3 supplementation to improve glucose homeostasis in patients with T2D.

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Tags: Diabetes