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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
Published on: June 28, 2024
Biometric Alterations of Mouse Embryonic Eye Structures Due to Short-Term Folic Acid Deficiency
Ouafa Sijilmassi1,2, José Manuel López-Alonso2, Aurora Del Río Sevilla1
1a Faculty of Optics and Optometry, Anatomy and Human Embryology Department , Universidad Complutense De Madrid , Madrid , Spain.
Insights
Maternal folic acid deficiency (FAD) in mice causes smaller eyes and lenses, and a larger retina in offspring. Even short-term FAD impacts embryonic ocular development.
Area of Science:
- Developmental biology
- Ophthalmology
- Nutritional science
Background:
- Folic acid (FA) is crucial for embryonic development, with deficiency linked to neural tube defects.
- The impact of maternal FA deficiency (FAD) on ocular development is not well understood.
- The eye originates from the neural tube, suggesting a potential link between FAD and eye formation.
Purpose of the Study:
- To investigate the effects of maternal FAD on ocular biometry in mouse embryos.
- To analyze how different durations of FAD exposure influence eye development.
Main Methods:
- Female mice were assigned to control (standard FA diet), short-term FAD, or long-term FAD groups.
- Embryos (n=57) were collected at 14.5 gestational days for ocular biometry analysis.
- ImageJ software was used to measure the area of the lens, eye, and retina, along with their circularity.
Main Results:
- Embryos from FAD groups exhibited smaller lenses and eyes compared to controls.
- Long-term maternal FAD led to a spatially increased neural retina size.
- Eyes and lenses in FAD-exposed embryos showed increased circularity.
Conclusions:
- Maternal FAD, even for a short term, induces morphological alterations in offspring ocular structures.
- Folic acid is essential for normal embryonic eye development.
- Dietary interventions during pregnancy can significantly impact fetal eye development.
Purpose:
Folic acid (FA) is an essential nutrient for normal embryonic development. FA deficiency (FAD) in maternal diet increases the risk of several defects among the progeny, especially, neural tube defects. The eye begins its development from the neural tube; however, the relationship between FAD and ocular development in the offspring has been little explored and it isn't known how the FAD affects the formation of the eye. Our objective was to analyze the effect of maternal FAD on mouse embryos ocular biometry.
Methods:
Female mice C57/BL/6J were distributed into three different groups, according to the assigned diet: control group fed a standard FA diet (2 mg FA/kg), FAD group for short term fed (0 mg FA/kg + 1% succinylsulfathiazole) from the day after mating until day 14.5 of gestation, and FAD group for long term fed the same FA-deficient diet for 6 weeks prior mating and continued with this diet during gestation. A total of 57 embryos (19 embryos of each dietary group) at 14.5 gestational days were evaluated. As indicators of changes in ocular biometry, we analyze two parameters: area and circularity of the lens and whole eye, and the area of the retina. The program used in the treatment and selection of the areas of interest was ImageJ. The statistical analysis was performed by IBM SPSS Statistics 19.
Results:
Regarding the measures of the area, FA-deficient lenses and eyes were smaller than that of controls. We have also observed increase in the size of the neural retina, spatially, in embryos from females fed FAD diet during long term. On the other hand, as regard to circularity measures, we have seen that eyes and lenses were more circular than control.
Conclusion:
Maternal FAD diet for a very short term generates morphological changes in ocular structures to the offspring.
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