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Updated: May 14, 2026
Modifying Levels of Maternal Dietary Folic Acid or Choline to Study the Impact of Deficiencies on Offspring Health Outcomes
Published on: June 28, 2024
Insufficient ascorbic acid intake during gestation induces abnormal cardiac dilation in fetal and neonatal SMP30/GNL
Yuki Kishimoto1, Takao Kanai, Kayoko Sato
1Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
Insights
Maternal ascorbic acid (AA) is crucial for fetal development. Insufficient AA during pregnancy in mice led to fetal death or severe developmental abnormalities in neonates, highlighting the need for adequate AA intake.
Area of Science:
- Reproductive biology
- Developmental biology
- Nutritional science
Background:
- Ascorbic acid (AA) is vital for pregnancy and fetal growth, but its exact role is unclear.
- Senescence marker protein-30/gluconolactonase (SMP30/GNL) knockout mice cannot synthesize AA, making them a model to study AA deficiency.
Purpose of the Study:
- To investigate the impact of maternal ascorbic acid (AA) levels on fetal mouse growth during gestation.
- To utilize SMP30/GNL knockout mice to examine the consequences of in vivo AA synthesis absence.
Main Methods:
- SMP30/GNL knockout mice were subjected to absent, low, or normal AA intake during gestation.
- AA levels were quantified using high-performance liquid chromatography with electrochemical detection.
- Fetal and neonatal tissues were analyzed via histological staining (H&E, EVG, Azan).
Main Results:
- Complete absence of maternal AA resulted in failed pregnancies due to incomplete fetal development.
- Neonates from mothers with low AA intake exhibited mortality within days, showing cardiac dilation, organ congestion, and skeletal defects.
- Normal AA intake by mothers led to healthy offspring development.
Conclusions:
- Sufficient ascorbic acid (AA) intake during gestation is essential for normal fetal and neonatal tissue development.
- This study underscores the critical role of maternal AA in preventing developmental abnormalities and ensuring offspring viability.
Background:
Despite the acknowledged importance of ascorbic acid (AA) in maintaining pregnancy and normal fetal development, its precise actions remain obscure. Therefore, we investigated the impact of maternal AA content on the growth of fetal mice during the gestation period using senescence marker protein-30/gluconolactonase (SMP30/GNL) knockout (KO) mice, which cannot synthesize AA in vivo.
Methods:
SMP30/GNL KO mice gave birth after a gestation period under conditions of absent, low, or normal AA intake. AA was measured using high-performance liquid chromatography and electrochemical detection. Whole-body sections were stained with hematoxylin and eosin, Elastica van Gieson, and Azan.
Results:
The mothers in the group absent AA intake failed to bear young because of incomplete fetal development. Offspring born under the low-AA condition generally died within a few days after birth. Morphological analysis revealed that the latter neonates of SMP30/GNL KO mothers whose intake of AA was low during gestation manifested abnormal cardiac dilation, congestion of the liver and lungs, incompletely expanded pulmonary alveoli, and impaired vertebral bodies. In contrast, a normal AA diet produced healthy progeny.
Conclusion:
A diet sufficiently replete with AA is essential during the gestational period for normal tissue development in the fetus and neonate.
