Zumbro, Emily L.Guerin, Gena D.Gordon, Ryan A.White, Chase M.McAdams, Dreanna M.Sokoloski, Matthew L.Nichols, David L., Ph. D.Duplanty, Anthony A.2020-09-182020-09-182020https://hdl.handle.net/11274/12492Creative Arts and Research SymposiumSkeletal muscle (SKM) is an important regulator of metabolism with thyroid hormone (TH) being an important factor in mitochondrial biogenesis. PURPOSE: The purpose of this study was to explore mitochondrial dysregulation in a hypothyroid In Vitro model and examine the influence of an exercise mimetic, formoterol, on this pathway. METHODS: SKM myoblasts were TH depleted (ThD), ThD plus formoterol stimulation (ThD+F), or control cells (CON) with total RNA extracted during mid-myogenesis (D4) and at terminal differentiation (D6). Gene expression for PGC-1α, TFAM, and NRF1 was analyzed by qPCR. RESULTS: ThD media resulted in reduced NRF1 and TFAM. ThD+F resulted in increased PGC-1α (regulator of mitochondrial biogenesis) but decreased expression of its downstream targets TFAM and NRF1. CONCLUSION: Formoterol increases initial stimulation of mitochondrial biogenesis (PGC-1α) but related downstream signaling is decreased by TH depletion (TFAM and NRF1). This suggests that overall exercise signaling may be impaired by Hypothyroidism.en-USPoster