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Thyroid hormones, including 3,5,3'-triiodothyronine (T 3 ), cause a wide spectrum of genomic effects on cellular metabolism and bioenergetic regulation in various tissues. The non-genomic actions of T 3 have been reported but are not yet completely understood. Acute T 3 treatment significantly enhanced basal, maximal, ATP-linked, and proton-leak oxygen consumption rates (OCRs) of primary differentiated mouse brown adipocytes accompanied with increased protein abundances of uncoupling protein 1 (UCP1) and mitochondrial Ca 2+ uniporter (MCU). T 3 treatment depolarized the resting mitochondrial membrane potential (Ψ m ) but augmented oligomycin-induced hyperpolarization in brown adipocytes. Protein kinase B (AKT) and mammalian target of rapamycin (mTOR) were activated by T 3 , leading to the inhibition of autophagic degradation. Rapamycin, as an mTOR inhibitor, blocked T 3 -induced autophagic suppression and UCP1 upregulation. T 3 increases intracellular Ca 2+ concentration ([Ca 2+ ] i ) in brown adipocytes. Most of the T 3 effects, including mTOR activation, UCP1 upregulation, and OCR increase, were abrogated by intracellular Ca 2+ chelation with BAPTA-AM. Calmodulin inhibition with W7 or knockdown of MCU dampened T 3 -induced mitochondrial activation. Furthermore, edelfosine, a phospholipase C (PLC) inhibitor, prevented T 3 from acting on [Ca 2+ ] i , UCP1 abundance, Ψ m , and OCR. We suggest that short-term exposure of T 3 induces UCP1 upregulation and mitochondrial activation due to PLC-mediated [Ca 2+ ] i elevation in brown adipocytes.

Thyroid Hormone Induces Ca2+-Mediated Mitochondrial Activation in Brown Adipocytes