Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Ontogenesis of thyroid function and interactions with maternal function.

M J Obregon1, R M Calvo, F Escobar Del Rey

  • 1Instituto de Investigaciones Biomedicas, Centro mixto 'Alberto Sols' (CSIC-UAM), Madrid, Spain.

Endocrine Development
|August 9, 2007
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Late maternal hypothyroidism alters the expression of Camk4 in neocortical subplate neurons: a comparison with Nurr1 labeling.

Cerebral cortex (New York, N.Y. : 1991)·2013
Same author

Role of late maternal thyroid hormones in cerebral cortex development: an experimental model for human prematurity.

Cerebral cortex (New York, N.Y. : 1991)·2009
Same author

Tri-iodothyronine upregulates adiponutrin mRNA expression in rat and human adipocytes.

Molecular and cellular endocrinology·2009
Same author

Clinical dilemmas arising from the increased intake of iodine in the Spanish population and the recommendation for systematic prescription of potassium iodide in pregnant and lactating women (Consensus of the TDY Working Group of SEEN).

Journal of endocrinological investigation·2009
Same author

Thermogenic effect of triiodothyroacetic acid at low doses in rat adipose tissue without adverse side effects in the thyroid axis.

American journal of physiology. Endocrinology and metabolism·2008
Same author

Transthyretin is not necessary for thyroid hormone metabolism in conditions of increased hormone demand.

The Journal of endocrinology·2005

Maternal thyroxine (T4) is crucial for fetal brain development, with its transfer protecting neurodevelopment until birth. Prompt treatment of maternal thyroid issues and continued T4 transfer are vital for preventing neurodevelopmental deficits.

Area of Science:

  • Endocrinology
  • Neuroscience
  • Developmental Biology

Background:

  • Fetal thyroid function development involves gland and hypothalamic-pituitary-thyroid axis maturation.
  • Maternal thyroxine (T4) transfer is essential for fetal brain protection starting early in gestation.
  • Thyroid hormone metabolism and its impact on neurodevelopment are critical areas of study.

Purpose of the Study:

  • To review the role of thyroid hormones in fetal neurodevelopment.
  • To highlight the importance of maternal thyroxine transfer for the developing fetal brain.
  • To discuss the consequences of maternal thyroid dysfunction on neurodevelopment.

Main Methods:

  • Literature review focusing on thyroid hormone transfer and neurodevelopment.
  • Analysis of studies on fetal and neonatal thyroid function.

Related Experiment Videos

  • Examination of animal models and human epidemiological data.
  • Main Results:

    • Maternal thyroxine (T4) transfer significantly protects the fetal brain throughout gestation.
    • Free T4 levels in fetal fluids rise rapidly, influenced by maternal T4 levels.
    • Inadequate maternal T4 impacts neurodevelopment, as evidenced in rat models and human studies.

    Conclusions:

    • Maternal thyroxine is indispensable for normal fetal neurodevelopment.
    • Prompt treatment of maternal hypothyroidism/hypothyroxinemia is recommended.
    • Preterm infants may face neurodevelopmental issues due to interrupted maternal T4 transfer.