Effects of vitamin D and calcium supplementation on pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes: the Calcium and Vitamin D for Diabetes Mellitus (CaDDM) randomized controlled trial1234

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Background: A suboptimal vitamin D and calcium status has been associated with higher risk of type 2 diabetes in observational studies, but evidence from trials is lacking.

Objective: We determined whether vitamin D supplementation, with or without calcium, improved glucose homeostasis in adults at high risk of diabetes.

Design: Ninety-two adults were randomly assigned in a 2-by-2 factorial-design, double-masked, placebo-controlled trial to receive either cholecalciferol (2000 IU once daily) or calcium carbonate (400 mg twice daily) for 16 wk. The primary outcome was the change in pancreatic β cell function as measured by the disposition index after an intravenous-glucose-tolerance test. Other outcomes were acute insulin response, insulin sensitivity, and measures of glycemia.

Results: Participants had a mean age of 57 y, a body mass index (BMI; in kg/m2) of 32, and glycated hemoglobin (Hb A1c) of 5.9%. There was no significant vitamin D × calcium interaction on any outcomes. The disposition index increased in the vitamin D group and decreased in the no–vitamin D group (adjusted mean change ± SE: 300 ± 130 compared with −126 ± 127, respectively; P = 0.011), which was explained by an improvement in insulin secretion (62 ± 39 compared with −36 ± 37 mU · L−1 · min, respectively; P = 0.046). Hb A1c increased less, but nonsignificantly, in the vitamin D group than in the no–vitamin D group (0.06 ± 0.03% compared with 0.14 ± 0.03%, respectively; P = 0.081). There was no significant difference in any outcomes with calcium compared with no calcium.

Conclusion: In adults at risk of type 2 diabetes, short-term supplementation with cholecalciferol improved β cell function and had a marginal effect on attenuating the rise in Hb A1c. This trial was registered at clinicaltrials.gov as NCT00436475.

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From the Division of Endocrinology, Diabetes, and Metabolism, Tufts Medical Center, Boston, MA (JM, BD-H, and AGP); the Bone Metabolism Laboratory, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA (BD-H); the Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA (FBH); and the Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA (FBH).

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The contents of the article are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health, the US Department of Agriculture, or the Endocrine Fellows Foundation.

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Supported by the National Institutes of Health [NIH; research grant R01DK76092 (to AGP) funded by the National Institute of Diabetes and Digestive and Kidney Disease and the NIH Office of Dietary Supplements], the National Center for Research Resources (UL1 RR025752; to Tufts Medical Center), the US Department of Agriculture (Cooperative Agreement no. 58-1950-4-401; to BDH), and an Endocrine Fellows Foundation grant (to JM). Calcium carbonate pills and matching placebos were donated by GlaxoSmith-Kline (Parsippany, NJ).

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Address reprint requests and correspondence to AG Pittas, Division of Endocrinology, Diabetes, and Metabolism, Tufts Medical Center, Box 268, 800 Washington Street, #268, Boston, MA 02111. E-mail: [email protected].