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Objectives Vitamin D deficiency was associated with obesity. However, the causal relationship remains controversial. We hypothesized that there would be family-based associations in both vitamin D deficient families and obese families for the SNPs associated with vitamin D deficiency, if vitamin D deficiency was a causal factor of obesity. We aimed to investigate the family-based association of SNPs in CYP27B1 with both vitamin D deficiency and obesity. Methods Four hundred and nineteen pedigrees containing 1505 rural individuals aged from 18 to 79 years in Henan Province of China were included in this study. Family-based associations of rs10877012 and rs4646536 in CYP27B1 with vitamin D deficiency and obesity were investigated. Serum 25(OH)D3 concentration Results It was shown that vitamin D deficiency was a risk factor of obesity (adjusted OR: 1.332, 95% CI: 1.042-1.703, P = 0.022). Furthermore, there were family-based associations for allele T of rs10877012 and allele T of rs4646536 in both vitamin D deficient families and obese families (P < 0.05). Both rs10877012 and rs4646536 were associated with serum 25(OH)D3 levels between siblings (P < 0.05), but not BMI (P > 0.05). In addition, there is linkage disequilibrium between rs10877012 and rs4646536 (D' = 1.0, r.sup.2 = 0.992). Conclusion Vitamin D deficiency may be a causal factor of obesity. Maintaining sufficient vitamin D is beneficial to obesity prevention. Vitamin D deficiency was associated with obesity. But their causal relationship is still controversial. CYP27B1 plays a direct role in circulating the concentration of 25(OH)D, which can be used to investigate causal relationships. In this study, allele T of rs10877012 and allele T of rs4646536 in CYP27B1 were family-based linked with both vitamin D deficiency and obesity. In addition, both rs10877012 and rs4646536 were associated with serum 25(OH)D.sub.3 levels between siblings but not BMI. Therefore, vitamin D deficiency may be a causal factor of obesity. Maintaining sufficient vitamin D is beneficial to obesity prevention., Author(s): Songcheng Yu [sup.1], Yinhua Feng [sup.1], Chenling Qu [sup.2], Wenqian Huo [sup.1], Zhenxing Mao [sup.1], Chongjian Wang [sup.1], Wenjie Li [sup.1], Xing Li [sup.1] Author Affiliations: (1) College of [...]

Background: Physical activity and vitamin D receptor (VDR) have been associated with type 2 diabetes mellitus (T2DM). However, the associations of VDR methylation with T2DM and physical activity remained unknown. We aimed to investigate whether VDR methylation was a link between physical activity and T2DM. Methods: A 1:1 matching case‐control study was designed based on the Henan Rural Cohort Study, including 272 pairs of T2DM patients and nonpatients. Physical activity level was assessed using the International Physical Activity Questionnaire. The high‐resolution melt method was applied to determine the methylation level of the promoter region of VDR. The association between physical activity and T2DM was analyzed with a conditional logistic regression model. The effect modification of VDR methylation levels on the association between physical activity and T2DM was conducted. A multivariate correlation analysis model was applied to investigate correlations of VDR methylation with insulin sensitivity. Results: Physical activity level was associated with T2DM risk (crude model: odds ratio [OR] 0.611; 95% CI, 0.416‐0.897; adjusted model: OR 0.619; 95% CI, 0.418‐0.917). In effect modification analysis, the effects of physical activity on T2DM were stronger for low VDR methylation levels than for high (P =.025). Moreover, VDR methylation levels were associated with insulin (r = −0.089, P =.039) as well as homeostatic model assessment of insulin resistance (r = −0.098, P =.022). Conclusions: The methylation status of the VDR promoter is associated with the secretion and sensitivity of insulin. VDR methylation attenuates the association between physical activity and T2DM, indicating that proactively physical activity may reduce the risk of T2DM, especially in people with low VDR methylation level. [ABSTRACT FROM AUTHOR]