Epigenetic Reduction in Invariant NKT Cells following In Utero Vitamin D Deficiency in Mice

Background: Previous studies have shown the relationship between in utero lung development and vitamin D [25(OH)D], but there have been no studies to investigate whether vitamin D deficiency is a risk factor for respiratory distress syndrome (RDS) in preterm babies. Objectives: In this study, we investigated if 25(OH)D deficiency is a risk factor for RDS. Methods: One hundred fifty-two preterm newborns, born at 29 - 35 weeks gestational age, were included in the study following informed consent from the parents. Peripheral blood samples were collected within the first 24 hours of life and 25(OH)D levels were measured by liquid chromatography-tandem mass spectrometry. Demographic characteristics of the babies and the diagnosis of RDS were recorded. Results: In 64 % of preterm infants, 25(OH)D levels were compatible with severe deficiency (≤ 10 ng/mL), 33 % with moderate deficiency (10 - 20 ng/mL), and 3 % with mild deficiency (20 - 30 ng/mL). In none of the babies was a normal 25(OH)D level observed. Serum 25(OH)D levels were not correlated with gestational age. Respiratory distress syndrome was more common in preterm babies with severe (28 %) compared to mild-moderate 25(OH)D deficiency (14 %) (p < 0.05). Conclusions: None of the preterm infants in this study had normal vitamin D level, which underlined the burden of vitamin D deficiency in pregnant women and their offspring. RDS was more common in severely vitamin D-deficient preterms. Determination of vitamin D status of the mothers and appropriate supplementation might be a valuable strategy to reduce RDS, in addition to antenatal steroids. Besides, since vitamin D is a regulatory factor in many organs during fetal development, long-term effects of in utero vitamin D deficiency warrant further studies.

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In utero vitamin D deficiency predisposes offspring to long-term adverse adipose tissue effects

Journal of Endocrinology ◽

10.1530/joe-17-0015 ◽

2017 ◽

Vol 234 (3) ◽

pp. 301-313 ◽

Cited By ~ 8

Author(s):

Anthony M Belenchia ◽

Sarah A Johnson ◽

Mark R Ellersieck ◽

Cheryl S Rosenfeld ◽

Catherine A Peterson

Keyword(s):

Metabolic Disease ◽

Vitamin D ◽

Adipose Tissue ◽

Vitamin D Deficiency ◽

In Utero ◽

Metabolic Health ◽

Health Concern ◽

Rapid Weight Gain ◽

Postnatal Environment

The fetal period represents an important window of susceptibility for later obesity and metabolic disease. Maternal vitamin D deficiency (VDD) during pregnancy is a global concern that may have long-lasting consequences on offspring metabolic health. We sought to determine whether a VDD in utero environment affects fetal adipose tissue development and offspring metabolic disease predisposition in adulthood. Furthermore, we sought to explore the extent to which the VDD intrauterine environment interacts with genetic background or postnatal environment to influence metabolic health. Eight-week-old P0 female C57BL/6J mice were fed either a VDD diet or sufficient diet (VDS) from four weeks before pregnancy (periconception) then bred to male Avy/a mice. Females were maintained on the diets throughout gestation. At weaning, Avy/a and a/a male F1 offspring were randomized to low-fat (LFD) or high-fat diet (HFD) until 19 weeks of age, at which point serum and adipose tissue were harvested for analyses. Mice born to VDD dams weighed less at weaning than offspring born to VDS dams but experienced rapid weight gain in the four weeks post weaning, and acquired a greater ratio of perigonadal (PGAT) to subcutaneous (SQAT) than control offspring. Additionally, these mice were more susceptible to HFD-induced adipocyte hypertrophy. Offspring of VDD dams also had greater expression of Pparg transcript. These novel findings demonstrate that in utero VDD, an easily correctable but highly prevalent health concern, predisposes offspring to long-term adipose tissue consequences and possible adverse metabolic health complications.

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