Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth.

08:00 EDT 28th September 2019 | BioPortfolio

Summary of "Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth."

Inappropriate intake of key micronutrients in pregnancy is known to alter maternal endocrine status, impair placental development and induce fetal growth restriction. Selenium is an essential micronutrient required for the function of approximately 25 important proteins. However, the specific effects of selenium deficiency during pregnancy on maternal, placental and fetal outcomes is poorly understood. This study demonstrates that maternal selenium deficiency increases maternal T and T , concentrations, reduces fetal blood glucose concentrations and induces fetal growth restriction. Placental expression of key selenium dependent thyroid hormone converting enzymes were reduced, while the expression of key placental nutrient transporters was dysregulated. Selenium deficiency had minimal impact on selenium dependent antioxidants but increased placental copper concentrations and expression of SOD1. These results highlight the idea that selenium deficiency during pregnancy may contribute to thyroid dysfunction, causing reduced fetal growth that likely precedes programmed disease outcomes in offspring.


Journal Details

This article was published in the following journal.

Name: The Journal of physiology
ISSN: 1469-7793


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Medical and Biotech [MESH] Definitions

A selenium compound used as a source of SELENIUM, especially for patients that develop selenium deficiency following prolonged PARENTERAL NUTRITION.

Pregnancy in which the mother and/or FETUS are at greater than normal risk of MORBIDITY or MORTALITY. Causes include inadequate PRENATAL CARE, previous obstetrical history (ABORTION, SPONTANEOUS), pre-existing maternal disease, pregnancy-induced disease (GESTATIONAL HYPERTENSION), and MULTIPLE PREGNANCY, as well as advanced maternal age above 35.

A condition in infancy or early childhood due to an in-utero deficiency of THYROID HORMONES that can be caused by genetic or environmental factors, such as thyroid dysgenesis or HYPOTHYROIDISM in infants of mothers treated with THIOURACIL during pregnancy. Endemic cretinism is the result of iodine deficiency. Clinical symptoms include severe MENTAL RETARDATION, impaired skeletal development, short stature, and MYXEDEMA.

Maternal deaths resulting from complications of pregnancy and childbirth in a given population.

Glycoproteins with the electrophoretic mobility of BETA-GLOBULINS, secreted by the placental TROPHOBLASTS into the maternal bloodstream during PREGNANCY. They can be detected 18 days after OVULATION and reach 200 mg/ml at the end of pregnancy. They are associated with fetal well-being.

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