Impact of mild iodine deficiency during gestation and/or lactation on embryonic thyroid development and the programming of thyroid dysfunctions throughout adulthood: an omics approach

• Grant number: 24/09333-7
• Support Opportunities: Regular Research Grants
• Start date: April 01, 2025
• End date: March 31, 2028
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Caroline Serrano Do Nascimento
• Grantee: Caroline Serrano Do Nascimento
• Host Institution: Instituto de Ciências Ambientais, Químicas e Farmacêuticas (ICAQF). Universidade Federal de São Paulo (UNIFESP). Campus Diadema. Diadema , SP, Brazil
• Associated researchers: Leonardo Vinícius Monteiro de Assis ; Maria Nathália de Carvalho Magalhães Moraes Figueira Borges

Abstract

Iodine is an essential micronutrient for the biosynthesis of thyroid hormones (TH), crucial for embryonic development. The detrimental effects of severe iodine deficiency during pregnancy and/or lactation are clearly described in the literature. However, the consequences of mild deficiency of this micronutrient are not fully elucidated. Even so, it is known that mild iodine deficiency during pregnancy and lactation is a reality in many countries, including Brazil, and occurs even in regions with an adequate supply of this micronutrient. Animal model studies have demonstrated the negative impact of this deficiency on the development of the central nervous system. Still, there is no conclusive data on the effects on the function of the hypothalamic-pituitary-thyroid axis in the progeny at different stages of development or in other tissues responsive to TH actions. Therefore, this study aims to investigate the impact of mild iodine deficiency during pregnancy and/or lactation on the embryonic development of the thyroid, the programming of thyroid dysfunctions, and their consequences in peripheral tissues during the adult life of the progeny animals. In vivo models, such as pregnant female mice and their progeny at different developmental stages, and in vitro models, such as embryonic stem cells differentiated into endoderm and thyroid, will be used. Transcriptomic, proteomic, and epigenetic analyses will be conducted to identify the molecular mechanisms involved in the dysregulation of the hypothalamus-pituitary-thyroid axis and potential new targets in different tissues responsive to TH. The project will contribute to elucidating the impact of a frequent nutritional imbalance in pregnant and lactating women on the programming of dysfunctions in progeny individuals during different developmental stages. (AU)