Maternal hypothyroidism-developing dyslipidemia

What is it about?

Maternal thyroid hormones (THs) are essential for the developing newborns, especially the thermogenesis, lipogenesis, and lipid contents (fatty acids composition and phospholipids in the cell membrane). There is a link between the hypothyroidism and dyslipidemia. In subclinical hypothyroidism, dyslipidemia might be accompanied by the following: (1) elevations in the levels of triglycerides (TGs); (2) reductions in the levels of high-density lipoprotein cholesterol (HDL-C); (3) elevations in the levels of low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC); (4) decrease the ratio of cholesterol/TGs; (5) increase the levels of apolipoprotein B (ApoB); and (6) increase the levels of lipoprotein(a) [Lp(a)] and apolipoprotein(a) [apo(a)]. More importantly, the above disruptions can increase the risk of the cardiovascular diseases. In fact, any change in the activities of the thyroid gland can be harmful to the body mass index (BMI) and cause obesity. Thus, I hypothesized the following: (1) THs, perhaps of maternal origin, play vital roles in the homeostasis of the fetal lipid profile; (2) the maternal thyroid disorders (hypothyroidism) may perturb the lipid homeostasis (contents, metabolism and distributions) in liver and adipose tissues during the gestation and lactation; (3) the maternal hypothyroidism may cause fetal/neonatal dyslipidemia; and (4) the maternal hypothyroidism may delay the fetal/neonatal development. Thus, adjusting the levels of maternal, fetal and neonatal THs and thyroid-stimulating hormone (TSH) can easily prevent this disturbance during the gestation and lactation. Future studies are required to understand the connection between the genomic and non-genomic actions of THs during the abnormal conditions (hypothyroidism or hyperthyroidism during the gestation and lactation) and fetal dyslipidemia. This view will assist to prevent not only the thyroid dysfunction during the critical developmental periods but also the cardiovascular disease and obesity (predominant diseases in our life). Thus, the association between the molecular and developmental investigations is warranted.

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Why is it important?

I hypothesized the following: (1) THs, perhaps of maternal origin, play vital roles in the homeostasis of the fetal lipid profile; (2) the maternal thyroid disorders (hypothyroidism) may perturb the lipid homeostasis (contents, metabolism and distributions) in liver and adipose tissues during the gestation and lactation; (3) the maternal hypothyroidism may cause fetal/neonatal dyslipidemia; and (4) the maternal hypothyroidism may delay the fetal/neonatal development. Thus, adjusting the levels of maternal, fetal and neonatal THs and thyroid-stimulating hormone (TSH) can easily prevent this disturbance during the gestation and lactation.

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