No abstract

The review aims to summarize the available research focusing on the importance of monocarboxylate transporter (MCT8) in thyroid hormone trafficking across the placenta and fetal development. A systematic search was carried out in PubMed; studies available in English related to “monocarboxylate transporter”, “adverse pregnancy”, “fetal development,” and “thyroid hormone” were identified and assessed. The references within the resulting articles were manually searched. MCT8 is a highly active and selective thyroid hormone transporter that facilitates the cellular uptake of triiodothyronine (T3), thyroxine (T4), reverse triiodothyronine (rT3), and diiodothyronine (T2) in different tissues. MCT8 is expressed in the placenta from the first trimester onwards, allowing the transport of thyroid hormone from mother to fetus. Mutations in MCT8 cause an X-linked disorder known as Allan-Herndon-Dudley syndrome (AHDS), characterized by severe psychomotor impairment and peripheral thyrotoxicosis. Hence, any maternal thyroid dysfunction may cause severe consequences for the fetus and newborn. Further research regarding MCT8 gene expression, polymorphic variation, and adverse pregnancy outcomes must be done to establish that MCT8 is a novel prognostic marker for the early detection of pregnancy-related complications.

About 10 to 20% of reported pregnancies have complications like spontaneous abortion (SA), preeclampsia (PE), preterm birth (PTB), and fetal growth restriction (FGR);  60% are attributed to maternal nutritional alterations. Multiple micronutrients (MMN) are supplemented in the antenatal period, but no proper validation/guidelines are available regarding dosing/time, the need for initiation, and the duration of supplementation. Studies have reported adverse pregnancy complications related to the overuse/unwanted use of multiple micronutrient supplementations during pregnancy. Identifying the exact population requiring supplementation is necessary to prevent its abuse. This article attempts to review the impacts of micronutrient deficiency/supplementation in cases of SA, FGR, and gestational diabetes mellitus (GDM), preterm delivery and PE.  The study used a literature search using PubMed, Google Scholar, Mendeley, and Scopus Databases using search words pregnancy, spontaneous abortion, gestational diabetes mellitus (GDM), fetal growth restriction (FGR), preterm delivery, preeclampsia (PE) or “adverse pregnancy” associated with minerals, micronutrients, or supplementation. The review also considered in-house literature databases, a single-window search at Kasturba Medical College (KMC) Health sciences library, MAHE (Manipal Academy of Higher Education). The figures included in the study were created by Biorender.com. Micronutrients play multiple roles during pregnancy and fetoplacental growth stimulating growth hormone secretion, Lysyl oxidase (LOX), involved in the crosslinking between collagen and elastin in the amniotic membrane, downregulation of interleukin (IL)-1 alpha, IL-1 beta, IL-4, IL-6, Il-10, IL-12, tumor necrosis factor (TNF)-alpha and several chemokines involved in hypertension, immune-inflammatory pathways, attenuate insulin resistance a structural development of neurons and glia. Over-supplementation has led to complications such as spontaneous abortion and gestational diabetes mellitus. Since there is a lack of standardization concerning micronutrient supplementation during pregnancy, there is a need for  systematic study related to the role of micronutrients during each trimester of pregnancy to optimize its supplementation and to prevent hazards associated with its abuse.