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Prenatal programming of adult thyroid function by alcohol and thyroid hormones
Jennifer Slone Wilcoxon1, Eva E Redei
1Department of Psychiatry and Behavioral Sciences, Northwestern University Medical School, The Asher Center, Chicago, Illinois 60611, USA. jwilcoxo@bsd.uchicago.edu
American Journal of Physiology. Endocrinology and Metabolism
|April 29, 2004
Summary
Maternal alcohol consumption during pregnancy can permanently alter offspring thyroid function. Fetal alcohol exposure leads to decreased T3 and elevated TSH in adult rats, suggesting lasting thyroid programming.
Area of Science:
- Endocrinology
- Developmental Biology
- Neuroscience
Background:
- Early-life environmental exposures can cause permanent physiological changes in adulthood.
- Fetal programming describes adaptive fetal responses to the prenatal environment that impact adult physiology.
Purpose of the Study:
- To investigate the link between alcohol-induced maternal thyroid dysfunction and the hypothalamic-pituitary-thyroid (HPT) axis function in adult rat offspring.
- To determine if maternal thyroid hormone administration can mitigate alcohol's effects on offspring HPT function.
Main Methods:
- Assessed plasma levels of triiodothyronine (T3), thyroxine (T4), and thyroid-stimulating hormone (TSH) in pregnant dams and their offspring.
- Compared HPT function in adult offspring exposed to alcohol in utero versus control groups.
- Administered T4 to pregnant dams to evaluate its impact on maternal and offspring thyroid function.
Main Results:
- Alcohol-consuming dams showed decreased maternal T3, T4, and TSH.
- Adult offspring exposed to alcohol in utero (FAE) exhibited significantly lower T3 and higher TSH levels.
- Maternal T4 administration did not normalize the hypothyroid state in adult FAE offspring.
Conclusions:
- Maternal ethanol consumption alters HPT function, leading to persistent thyroid alterations in adult offspring.
- Prenatal exposure to ethanol can permanently program offspring thyroid function.
- Maternal T4 administration has complex effects on offspring thyroid function, influenced by diet and sex.