期刊
DIABETES
卷 60, 期 5, 页码 1624-1631出版社
AMER DIABETES ASSOC
DOI: 10.2337/db10-1656
关键词
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资金
- U.K. Medical Research Council (MRC) [G0000934]
- Wellcome Trust [068545/Z/02, 076113/C/04/Z, 076113, 079895]
- Wellcome Trust/Juvenile Diabetes Research Foundation [061858]
- National Institutes of Health Research of England
- Department of Health's National Institute for Health Research (Biomedical Research Centre)
- Medical Research Council [G0601653]
- Food Standards Agency
- Department of Health [4243]
- Juvenile Diabetes Research Foundation International
- National Institute for Health Research Cambridge Biomedical Centre
- European Union [241447, 201167]
- American Heart Association
- Medical Research Council [G0600717, G0601653, G0000934, G0400546, G0400546B] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0508-10274, PHCS/C4/4/016, NF-SI-0508-10275] Funding Source: researchfish
- MRC [G0400546, G0600717, G0000934, G0601653] Funding Source: UKRI
OBJECTIVE Vitamin D deficiency (25-hydroxyvitamin D [25(OH)D] < 50 nmol/L) is commonly reported in both children and adults worldwide, and growing evidence indicates that vitamin D deficiency is associated with many extraskeletal chronic disorders, including the autoimmune diseases type 1 diabetes and multiple sclerosis. RESEARCH DESIGN AND METHODS We measured 25(OH)D concentrations in 720 case and 2,610 control plasma samples and genotyped single nucleotide polymorphisms from seven vitamin D metabolism genes in 8,517 case, 10,438 control, and 1,933 family samples. We tested genetic variants influencing 25(OH)D metabolism for an association with both circulating 25(OH)D concentrations and disease status. RESULTS Type 1 diabetic patients have lower circulating levels of 25(OH)D than similarly aged subjects from the British population. Only 4.3 and 18.6% of type 1 diabetic patients reached optimal levels (>= 75 nmol/L) of 25(OH)D for bone health in the winter and summer, respectively. We replicated the associations of four vitamin D metabolism genes (GC, DHCR7, CYP2R1, and CYP24A1) with 25(OH)D in control subjects. In addition to the previously reported association between type 1 diabetes and CYP27B1 (P = 1.4 x 10(-4)), we obtained consistent evidence of type 1 diabetes being associated with DHCR7 (P = 1.2 x 10(-3)) and CYP2R1 (P = 3.0 x 10(-3)). CONCLUSIONS Circulating levels of 25(OH)D in children and adolescents with type 1 diabetes vary seasonally and are under the same genetic control as in the general population but are much lower. Three key 25(OH)D metabolism genes show consistent evidence of association with type 1 diabetes risk, indicating a genetic etiological role for vitamin D deficiency in type 1 diabetes. Diabetes 60:1624-1631, 2011
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