L L N Husemoen1, T Skaaby1, T Martinussen2, T Jørgensen3, B H Thuesen1, C Kistorp4, J Jeppesen5, J P Thyssen6, M Meldgaard7, P B Szecsi7, M Fenger8, A Linneberg1. 1. Research Centre for Prevention and Health, Copenhagen University Hospital Glostrup, Glostrup, Denmark. 2. Department of Biostatistics, University of Copenhagen, Copenhagen, Denmark. 3. 1] Research Centre for Prevention and Health, Copenhagen University Hospital Glostrup, Glostrup, Denmark [2] Faculty of Health Science, University of Copenhagen, Copenhagen, Denmark. 4. Department of Cardiology and Endocrinology, Copenhagen University Hospital Frederiksberg, Frederiksberg, Denmark. 5. 1] Faculty of Health Science, University of Copenhagen, Copenhagen, Denmark [2] Department of Medicine M, Copenhagen University Hospital Glostrup, Glostrup, Denmark. 6. National Allergy Research Centre, Department of Dermato Allergology, Copenhagen University Hospital Gentofte, Hellerup, Denmark. 7. Department of Clinical Biochemistry, Copenhagen University Hospital Gentofte, Hellerup, Denmark. 8. Department of Clinical Biochemistry, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark.
Abstract
BACKGROUND/ OBJECTIVES: The aim was to examine the causal effect of vitamin D on serum adiponectin using a multiple instrument Mendelian randomization approach. SUBJECTS/ METHODS: Serum 25-hydroxy vitamin D (25(OH)D) and serum total or high molecular weight (HMW) adiponectin were measured in two Danish population-based studies: the Inter99 study (6405 adults, 30-60 years) conducted in 1999-2001, and the MONICA10 study (2656 adults, 41-71 years) conducted in 1993-1994. RESULTS: In the Inter99 study, serum 25(OH)D was positively associated with total adiponectin (the effect estimate in % per doubling of 25(OH)D was 4.78, 95% CI: 1.96, 7.68, P<0.001). Using variations in the vitamin D-binding protein gene and the filaggrin gene as instrumental variables, the causal effect in % was estimated to 61.46, 95% CI: 17.51, 120.28, P=0.003 higher adiponectin per doubling of 25(OH)D. In the MONICA10 cohort, no significant association was observed between the serum concentrations of 25(OH)D and HMW adiponectin (the effect estimate in % per doubling of 25(OH)D was -1.51, 95% CI: -5.80, 2.98, P=0.50), although the instrumental variables analysis to some extent supported a positive causal association (the effect estimate in % per doubling of 25(OH)D was 37.13, 95% CI: -3.67, 95.20, P=0.080). CONCLUSIONS: The results indicate a possible causal association between serum 25(OH)D and total adiponectin. However, the association was not replicated for HMW adiponectin. Thus, further studies are needed to confirm a causal relationship.
BACKGROUND/ OBJECTIVES: The aim was to examine the causal effect of vitamin D on serum adiponectin using a multiple instrument Mendelian randomization approach. SUBJECTS/ METHODS: Serum 25-hydroxy vitamin D (25(OH)D) and serum total or high molecular weight (HMW) adiponectin were measured in two Danish population-based studies: the Inter99 study (6405 adults, 30-60 years) conducted in 1999-2001, and the MONICA10 study (2656 adults, 41-71 years) conducted in 1993-1994. RESULTS: In the Inter99 study, serum 25(OH)D was positively associated with total adiponectin (the effect estimate in % per doubling of 25(OH)D was 4.78, 95% CI: 1.96, 7.68, P<0.001). Using variations in the vitamin D-binding protein gene and the filaggrin gene as instrumental variables, the causal effect in % was estimated to 61.46, 95% CI: 17.51, 120.28, P=0.003 higher adiponectin per doubling of 25(OH)D. In the MONICA10 cohort, no significant association was observed between the serum concentrations of 25(OH)D and HMW adiponectin (the effect estimate in % per doubling of 25(OH)D was -1.51, 95% CI: -5.80, 2.98, P=0.50), although the instrumental variables analysis to some extent supported a positive causal association (the effect estimate in % per doubling of 25(OH)D was 37.13, 95% CI: -3.67, 95.20, P=0.080). CONCLUSIONS: The results indicate a possible causal association between serum 25(OH)D and total adiponectin. However, the association was not replicated for HMW adiponectin. Thus, further studies are needed to confirm a causal relationship.
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