Hanson, Benjamin2025-03-212025-03-212024-12https://hdl.handle.net/11299/270539University of Minnesota M.S. thesis. December 2024. Major: Integrated Biosciences. Advisor: Grant Anderson. 1 computer file (PDF); vi, 96 pages.Thyroid hormone deficiency and iron deficiency are two prevalent nutritional disorders that significantly impact neonatal development, particularly in the context of brain. This study investigates the unique and overlapping effects of these deficiencies on gene expression in the context of neurodevelopment. Our findings reveal that TH deficiency leads to the downregulation of several key genes involved in peroxisomal lipid metabolism, particularly those associated with beta-oxidation. This downregulation compromises the liver's capacity to oxidize fatty acids, resulting in reduced ketone body production. Similarly, iron deficiency triggers a metabolic switch from fatty acid beta-oxidation to glycolytic dependence, with significant downregulation of genes involved in ketogenesis and upregulation of glycolytic genes. We also found that there is a compounded effect on myelination and extracellular matrix organization, essential for neuronal connectivity and function. Notably, the study highlights the role of insulin-like growth factor signaling, which is significantly perturbed in both deficiencies, linking liver function to neurodevelopmental outcomes. The implications of these findings underscore the necessity for early detection and intervention strategies in populations at risk for TH and iron deficiencies, particularly in neonates. Future research should focus on elucidating the molecular mechanisms underlying these interactions and their long-term impacts on cognitive and motor development.eniron deficiencyneonatal developementrna sequencingThyoid hormoneThesis or Dissertation