Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Echinobase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
Echinobase
ECB-ART-52600
Mol Cell Endocrinol 2023 Oct 18;579:112086. doi: 10.1016/j.mce.2023.112086.
Show Gene links Show Anatomy links

Thyroid dysfunction alters gene expression of proteins related to iron homeostasis and metabolomics in male rats.

da Conceição RR , Giannocco G , Herai RH , Petroski LP , Pereira BG , Oliveira KC , Chiamolera MI , Sato MA , Maciel RM , de Souza JS .


Abstract
Thyroid hormones (THs) are crucial in bodily functions, while iron is essential for processes like oxygen transport. Specialized proteins maintain iron balance, including ferritin, transferrin, ferroportin, and hepcidin. Research suggests that THs can influence iron homeostasis by affecting mRNA and protein expression, such as ferritin and transferrin. Our study focused on male rats to assess mRNA expression of iron homeostasis-related proteins and metabolomics in thyroid dysfunction. We found altered gene expression across various tissues (liver, duodenum, spleen, and kidney) and identified disrupted metabolite patterns in thyroid dysfunction. These findings highlight tissue-specific effects of thyroid dysfunction on essential iron homeostasis proteins and provide insights into associated metabolic changes. Our research contributes to understanding the intricate interplay between thyroid hormones and iron balance. By unveiling tissue-specific gene expression alterations and metabolic disruptions caused by thyroid dysfunction, our work lays a foundation for future investigations to explore underlying mechanisms and develop targeted strategies for managing iron-related complications in thyroid disorders.

PubMed ID: 37858610
Article link: Mol Cell Endocrinol