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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
Published on: June 28, 2024
Thyroid function alterations attributed to high iodide supplementation in maternal rats and their offspring.
Xue Liang1, Yanni Feng1, Laixiang Lin2
1Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
High iodide intake in maternal rats can lead to thyroid dysfunction and thyroiditis in both mothers and offspring. Even moderate high iodide levels (10x) in offspring can cause hypothyroidism and thyroiditis by adulthood.
Area of Science:
- Endocrinology
- Toxicology
- Reproductive Biology
Background:
- Iodide is essential for thyroid hormone synthesis, but excessive intake can disrupt thyroid function.
- Maternal thyroid status significantly impacts fetal and offspring development.
- Understanding the effects of high iodide supplementation is crucial for maternal and child health.
Purpose of the Study:
- To investigate the impact of high iodide supplementation during pregnancy and lactation on maternal and offspring thyroid function.
- To assess thyroid hormone levels, iodine content, oxidative stress, and gene expression in response to varying iodide intakes.
- To determine the long-term effects of prenatal and early-life iodide exposure on thyroid health in offspring.
Main Methods:
- Pregnant rats were divided into normal iodide intake (NI), 10x high iodide (10 HI), and 100x high iodide (100 HI) groups.
- Maternal urine, milk, thyroid, and mammary gland tissues were analyzed for iodine concentration, oxidative stress, and specific gene expression (TRα1, TRβ1, NIS, Dio1).
- Offspring were exposed to different iodide levels from weaning to postnatal day 180 (PN180), with serum thyroid hormones and antibodies measured.
Main Results:
- High iodide intake (10 HI and 100 HI) significantly increased iodine concentration in maternal tissues and milk.
- Maternal rats in the 100 HI group exhibited altered thyroid hormones (low FT3, high FT4), increased thyroid antibodies (TPOAb, TgAb), elevated mitochondrial superoxide production, and decreased expression of key thyroid-related genes.
- Offspring exposed to 10 HI and 100 HI showed decreased FT3 and FT4 levels, and increased TSH, TPOAb, and TgAb at PN180, indicating hypothyroidism and thyroiditis.
Conclusions:
- Maternal normal thyroid function can be maintained with 10x high iodide intake, but 100x high iodide intake induces thyroiditis during lactation.
- Offspring exposed to both 10x and 100x high iodide levels develop hypothyroidism complicated with thyroiditis by adulthood (PN180).
- Excessive iodide supplementation during gestation and lactation poses significant risks to maternal and offspring thyroid health, necessitating careful dosage monitoring.
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