4.7 Article

Association of vitamin D deficiency with incidence of type 2 diabetes in high-risk Asian subjects

Journal

AMERICAN JOURNAL OF CLINICAL NUTRITION
Volume 97, Issue 3, Pages 524-530

Publisher

OXFORD UNIV PRESS
DOI: 10.3945/ajcn.112.048496

Keywords

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Funding

  1. National Research Foundation
  2. Korean government [2006-2005410]
  3. Seoul National University Bundang Hospital
  4. Seoul Research & Business Development program, Republic of Korea [10526]
  5. National Institute for Diabetes and Digestive and Kidney Diseases (NIDDK) [K24 DK080140]
  6. Endocrine Society's Lilly Endocrine Scholar's Award
  7. NIH Loan Repayment Award
  8. NIDDK [1 L30 DK089944-01]
  9. Doris Duke Charitable Foundation
  10. National Research Foundation of Korea [2006-2005410] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Background: Recent studies suggest an association between 25-hydroxyvitamin D [25(OH)D] and type 2 diabetes (T2D) risk. However, prospective studies investigating the relation between vitamin D inadequacy and incidence of T2D incorporating obesity and dynamic measures of insulin resistance (IR) and pancreatic beta cell function are limited. Objective: We tested the hypothesis that baseline 25(OH)D is associated with the incidence of T2D in high-risk subjects for up to 5 y of follow-up, independently of obesity, baseline IR. and beta cell function. Design: We recruited 1080 nondiabetic Korean subjects [mean +/- SD age: 49.5 +/- 11.4 y] based on the presence of one or more risk factors for T2D, including obesity, hypertension, dyslipidemia, and/or family history of T2D. We measured anthropometric and biochemical indicators, HOMA2-IR, and the insulinogenic index (IGI; calculated as change in insulin at 30 min/change in glucose at 30 min) from a 75-g oral-glucose-tolerance test. Results: Of the participants, 10.5% had a serum 25(OH)D deficiency (<10 ng/mL), 51.6% had an insufficiency (10.0-19.9 ng/mL), and 38.0% had a sufficiency (>= 20 ng/mL), and the incidence of T2D at 32.3 +/- 15.6 mo (+/- SD) declined accordingly: 15.9%, 10.2%, and 5.4%, respectively (P < 0.001). After adjustment for age, sex, blood pressure, lifestyles, family history, season, parathyroid hormone, and high-sensitivity C-reactive protein, the participants with 25(OH)D deficiency had an increased risk of T2D independently of BMI, HOMA2-IR, and IGI; the HRs were 2.06 (95% CI: 1.22, 3.49) for 25(OH)D 10-19.9 ng/mL compared with >= 20 ng/mL and 3.23 (95% CI: 1.66, 6.30) for 25(OH)D <10 ng/mL compared with >= 20 ng/mL. Conclusion: The current prospective study suggests that vitamin D metabolism may play a role in T2D pathogenesis independently of known risk factors. This trial was registered at clinicaltrials.gov as NCT01508481. Am J Curt Nutr 2013;97:524-30.

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