AI Article Synopsis
- - Vitamin D deficiency (VDD) is a rising global concern linked to liver fat accumulation in adults, and this study examines its effects on the liver and lipid metabolism of adult offspring based on maternal VDD and diet types.
- - Researchers used various techniques, including liver histology and lipid analysis, and found that while VDD and a high-fat diet did not significantly affect liver structure in either males or females, male offspring of VDD mothers on a high-fat diet showed increased lipid levels and changes in lipid composition.
- - The study concludes that maternal VDD, particularly when paired with a high-fat diet, may lead to specific liver fat changes in male offspring, suggesting that maternal nutrition can influence liver health in future generations.
Article Abstract
Scope: Vitamin D deficiency (VDD) is becoming a global issue and low 25-hydroxyvitamin D (25(OH)D) plasma levels have been linked to hepatic steatosis in adulthood. Nevertheless, the impact of maternal VDD on lipid metabolism and hepatic steatosis remains poorly documented, especially under obesogenic condition. The goal of this study is to assess the effects of maternal VDD on hepatic lipid accumulation in adult offspring fed a normal or obesogenic diet.
Methods And Results: Several approaches are implemented including histology and lipidomics on the liver in both males and females. No major impact of high-fat (HF) or VDD is observed at histological level in both males and females. Nevertheless, in males born from VDD mice and fed an HF diet, an increase of total lipids and modulation of the relative lipid species distribution characterized by a decrease of triglycerides and increase of phospholipids is observed. In female no major lipid profile is noticed.
Conclusion: Maternal VDD combined with a HF diet in male may predispose to hepatic hypertrophia, with a specific lipid profile. Such observations reinforce our knowledge of the impact of maternal VDD on hepatic programming in the offspring.
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| http://dx.doi.org/10.1002/mnfr.202300290 | DOI Listing |
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