ArticleEndocrinology2016
Gene-by-Diet Interactions Affect Serum 1,25-Dihydroxyvitamin D Levels in Male BXD Recombinant Inbred Mice.
Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Is the vitamin D status of patients with COVID-19 associated with reduced mortality? A systematic review and meta-analysis.Archives of endocrinology and metabolism · 2023Pooled it
- Interindividual Genetic Differences Drive Discordance Between Serum Calcidiol and Calcitriol Concentrations in Females.Endocrinology · 2025Article
- The impact of inducible-whole body or intestine-specific Cyp24a1 gene knockout on vitamin D metabolism in mice.The Journal of steroid biochemistry and molecular biology · 2025Article
- Male Lrp5A214V mice maintain high bone mass during dietary calcium restriction by altering the vitamin D endocrine system.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Article
- Comprehensive identification of RNA transcripts and construction of RNA network in chronic obstructive pulmonary disease.Respiratory research · 2022Article
- Article
- Mechanistic study of the cause of decreased blood 1,25-Dihydroxyvitamin D in sepsis.BMC infectious diseases · 2019Observational
- FGF23 Synthesis and Activity.Current molecular biology reports · 2019Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
1,25-Dihydroxyvitamin D (1,25[OH]2D) regulates calcium (Ca), phosphate, and bone metabolism. Serum 1,25(OH)2D levels are reduced by low vitamin D status and high fibroblast growth factor 23 (FGF23) levels and increased by low Ca intake and high PTH levels. Natural genetic variation controls serum 25-hydroxyvitamin D (25[OH]D) levels, but it is unclear how it controls serum 1,25(OH)2D or the response of serum 1,25(OH)2D levels to dietary Ca restriction (RCR). Male mice from 11 inbred lines and from 51 BXD recombinant inbred lines were fed diets with either 0.5% (basal) or 0.25% Ca from 4 to 12 weeks of age (n = 8 per line per diet). Significant variation among the lines was found in basal serum 1,25(OH)2D and in the RCR as well as basal serum 25(OH)D and FGF23 levels. 1,25(OH)2D was not correlated to 25(OH)D but was negatively correlated to FGF23 (r = -0.5). Narrow sense heritability of 1,25(OH)2D was 0.67 on the 0.5% Ca diet, 0.66 on the 0.25% Ca diet, and 0.59 for the RCR, indicating a strong genetic control of serum 1,25(OH)2D. Genetic mapping revealed many loci controlling 1,25(OH)2D (seven loci) and the RCR (three loci) as well as 25(OH)D (four loci) and FGF23 (two loci); a locus on chromosome 18 controlled both 1,25(OH)2D and FGF23. Candidate genes underlying loci include the following: Ets1 (1,25[OH]2D), Elac1 (FGF23 and 1,25[OH]2D), Tbc1d15 (RCR), Plekha8 and Lyplal1 (25[OH]D), and Trim35 (FGF23). This report is the first to reveal that serum 1,25(OH)2D levels are controlled by multiple genetic factors and that some of these genetic loci interact with the dietary environment.
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