AI Article Synopsis

  • Vitamin D influences adipose tissue metabolism and has anti-inflammatory effects in adult mice, emphasizing its importance in fetal development to prevent future metabolic disorders.
  • This study examined how maternal vitamin D deficiency (VDD) affects inflammation in white adipose tissue of adult offspring, considering their diet (normal vs. high-fat).
  • Findings revealed that male offspring on a high-fat diet displayed increased inflammatory markers due to maternal VDD, specifically activating NF-kB signaling, while female offspring did not show significant changes.

Article Abstract

Vitamin D is acknowledged to play an important biological and metabolic role in adipose tissue, which is also the main storage site for this vitamin. Its anti-inflammatory effect in adipocytes and adipose tissue has notably been highlighted in adult mice. This vitamin is also crucial during fetal development since maternal vitamin D deficiency is suspected to program future metabolic disorders. Based on these observations, the aim of this study was to evaluate the consequences of maternal vitamin D deficiency (VDD) on white adipose tissue inflammation in adult offspring fed with normal or obesogenic diet (high-fat diet). White adipose tissue morphology, RNA and miRNA expression profiles, and signaling pathways were studied in adult males and females. In males, a HF diet coupled with maternal VDD increased expression of RNA and miRNA linked to inflammation leading to over-representation of inflammatory pathways. Interestingly, genomic and epigenetic profiles were associated with activation of the NF-kB signaling pathway and adiposity index. In females, no major modulation of inflammatory pathways was observed under VDD, contrarily to males. We concluded that maternal VDD coupled with HF diet activated inflammatory pathway in adipose tissue of the offspring, in a sex-dependent manner. Such activation is strongly related to activation of NF-kB signaling and increased adiposity only in males.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9265671PMC
http://dx.doi.org/10.3390/cells11132024DOI Listing

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