Premium
Maternal Vitamin D Deficiency Increases Intestinal Permeability and Programs Wnt/β‐Catenin Pathway in BALB/C Mice
Author(s) -
Yang Kefeng,
Zhu Jie,
Wu Jiang,
Zhong Yan,
Shen Xiuhua,
Petrov Brawnie,
Cai Wei
Publication year - 2021
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1002/jpen.1820
Subject(s) - offspring , endocrinology , medicine , wnt signaling pathway , vitamin a deficiency , intestinal permeability , vitamin , weaning , biology , vitamin d deficiency , vitamin d and neurology , signal transduction , pregnancy , microbiology and biotechnology , retinol , genetics
Abstract Background Recent studies suggest that vitamin D deficiency is associated with intestinal dysfunctions, but the underlying mechanism remains unclear. This study aimed to investigate whether maternal vitamin D deficiency increases intestinal permeability in offspring and its related mechanism. Methods Timed‐pregnant mice were fed with either a standard chow diet (SC) or a vitamin D–deprived chow diet (VD‐) 6 weeks prior to breeding and kept on the same diet until the end of gestation. All offspring were fed an SC for 3 weeks after weaning and then observed for effects associated with maternal vitamin D deficiency. Results Maternal vitamin D deficiency increased intestinal permeability in offspring, which corresponded with the decreased expression of the tight junction protein claudin‐1. Maternal vitamin D deficiency also repressed the messenger RNA expression of wingless/integrated family member 3a (Wnt3a) and the protein expression of nuclear β‐catenin. The decreased Wnt3a gene expression in male was concurrent with the changes in histone H4 acetylation at either promoter or coding regions. The activation of the Wnt/β‐catenin pathway protected against the impairment of intestinal permeability induced by maternal vitamin D deficiency. Conclusions Maternal vitamin D deficiency increased intestinal permeability and decreased tight junction protein expression in offspring. The suppression of the Wnt/β‐catenin signaling pathway through histone modification might be involved in the underlying mechanism.