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Maternal vitamin D deficiency increases the risk of obesity in male mice offspring by affecting the immune response

By Pei Li, Ping Li, Yuanlin Liu, Weijiang Liu, Lanlan Zha, Xiaoyu Chen, Rongxiu Zheng, Kemin Qi, Yi zhang

Posted 25 Mar 2020
bioRxiv DOI: 10.1101/2020.03.23.004721

Recently, many studies have indicated that obesity have their origin in the early stages of life, the objective of this study is to determine the risk of obesity in male mice offspring as a consequence of maternal VD deficiency-mediated disordering of the immune response. Four-week-old C57BL/6J female mice were fed VD-deficient or normal reproductive diets. Their male offspring were weighted and euthanized after being fed control and high-fat diets for 16 weeks. The serum was collected for biochemical analyses. Epididymal (eWAT) and inguinal (iWAT) white adipose tissues were excised for histological examination, immunohistochemistry, gene expressions and the proportions of immune cells. Insufficient maternal VD intake exacerbated the development of obesity as evidenced by larger adipose cells and abnormal glucose and lipid metabolisms. The expression of proinflammatory cytokine genes was increased and that of anti-inflammatory cytokines was decreased in maternal VD-deficient groups in the eWAT and/or iWAT. This was accompanied by higher levels of TNF-α or/and INF-γ, and lower levels of IL-4 and IL-10. Insufficient maternal VD intake was also observed to induce a shift in the profiles of immune cells in the eWAT and/or iWAT, resulting in increased percentages of M1 macrophage, ATDCs, and CD4+ and CD8+ T cells, but caused a significant decrease in the percentage of M2 macrophages. All these changes in the immune cell profile were more obvious in the eWAT than in the iWAT. These results indicated that insufficient maternal VD intake promoted the development of obesity in male offspring by modulating the immune cell populations.

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