Maternal transmission disequilibrium of rs2248359 in type 2 diabetes mellitus families and its association with vitamin D level in offspring.
Sci Rep. 2018 Jan 22;8(1):1345. doi: 10.1038/s41598-018-19838-5.
Yu S1, Li X1, Wang Y1, Mao Z1, Wang C1, Ba Y1, Li W2.
1 College of Public Health, Zhengzhou University, Zhengzhou, 450001, China.
2 College of Public Health, Zhengzhou University, Zhengzhou, 450001, China. Lwj at zzu.edu.cn.
- CYP24A1 gene and Vitamin D - many studies
- Diabetes changes liver genes so as to destroy (catabolize) Vitamin D – May 2016
- Genes such as CYP27B1, CYP24A1 and Vitamin D – JAMA Nov 2012
Items in both categories Diabetes and Genetics are listed here:
- DNA analysis of genes (Polygenic risk) shows increased risk of 9 health problems (all 9 fought by Vitamin D) – Feb 2024
- Increased Phosphorus increases Vitamin D getting to cells (CYP24A1, pigs) - Aug 2022
- Increased risk of diabetes if have poor Vitamin D genes – Dec 2020
- Poor CYP2R1 gene results in lower vitamin D and 2X increase in T1 Diabetes – Sept 2019
- Fasting and Diabetes both reduce Vitamin D activation (CYP2R1 in rodents) – May 2019
- Gestational Diabetes Mellitus associated with 4 Vitamin D genes – Oct 2015
- Diabetes changes liver genes so as to destroy (catabolize) Vitamin D – May 2016
- Low vitamin D in pregnancy – epigenetic pancreas problems in offspring (mice) – May 2016
- Diabetics with 8ng less vitamin D had a 50 percent increase chance of DHCR7 gene variation – Jan 2014
- Vitamin D receptor gene associated with 50 percent more type 2 Diabetes – meta-analyses 2013, 2016
- Fructose reduces blood levels of active vitamin D
- Type 1 diabetes, genes and vitamin D
- Vitamin D genes and insulin resistance – MS Aug 2010
notice CYP24A1 at the bottom of the chart -click on image for details
Download the PDF from VitaminDWiki
Association between T2DM and vitamin D deficiency has been reported in many epidemiologic studies. 24-hydroxylase encoded by CYP24A1 is the enzyme that degrades the active vitamin D metabolite. Variation in CYP24A1 may be associated with T2DM. This study investigates the association between rs2248359 in CYP24A1 and T2DM by a family-based association test (FBAT) and in a case-control study. The FBAT results revealed that there was transmission disequilibrium for allele T in both additive model (Z = 2.041, P = 0.041227) and dominant model (Z = 2.722, P = 0.006496). Results of the case-control study suggested that rs2248359 may be a risk factor for female T2DM (P = 0.036) but not for male T2DM (P = 0.816). Furthermore, excessive transmission of allele T in T2DM offspring was observed compared with the non-T2DM offspring (OR 1.392; 95%CI 1.024-1.894; P = 0.035). In addition, combination of maternal CT and paternal CC genotypes had significant synergistic effect on obtaining CT genotype for offspring with T2DM (OR 6.245; 95%CI 1.868-20.883; P = 0.004). Besides, lower level of 25(OH)D in T2DM offspring with genotype CT was observed as compared with the non-T2DM offspring (P = 0.013). These data suggest that maternal transmission disequilibrium of allele T may be a risk factor for T2DM and vitamin D deficiency in T2DM offspring.
PMID: 29358755 DOI: 10.1038/s41598-018-19838-5