Abstract
Thyroid hormone (TH) has diverse effects on mitochondria and energy expenditure (EE), generating great interest and research effort into understanding and harnessing these actions for the amelioration and treatment of metabolic disorders, such as obesity and diabetes. Direct effects on ATP utilization are a result of TH’s actions on metabolic cycles and increased cell membrane ion permeability. However, the majority of TH induced EE is thought to be a result of indirect effects, which, in turn, increase capacity for EE. This review discusses the direct actions of TH on EE, and places special emphasis on the indirect actions of TH, which include mitochondrial biogenesis and reduced metabolic efficiency through mitochondrial uncoupling mechanisms. TH analogs and the metabolic actions of T2 are also discussed in the context of targeted modulation of EE. Finally, clinical correlates of TH actions on metabolism are briefly presented.
Highlights
The maintenance of life is dependent on the metabolism of substrates in the form of carbohydrates, fats, and proteins to provide energy, and in the form of ATP to assure cell integrity and functions. in humans the day-to-day variations in energy flux are dramatic, over time, the dynamic equilibrium between energy intake (EI) and energy expenditure (EE) is remarkable
TH receptors (TRs) can exist as monomers, homodimers, and heterodimers; as heterodimers, they can interact with retinoid X receptor (RXR) or retinoic acid receptor (RAR) [44,45]
This is accomplished by uncoupling protein-1 (UCP1), which renders the inner membrane of the mitochondria permeable to electrons [64]
Summary
The maintenance of life is dependent on the metabolism of substrates in the form of carbohydrates, fats, and proteins to provide energy, and in the form of ATP to assure cell integrity and functions. Basal EE, otherwise defined as resting energy expenditure (REE), is the energy required to maintain basic cell and organ functions. Total EE (TEE) is defined as REE plus the energy consumed during activity (activity EE (AEE)) and diet-induced thermogenesis (DIT), the energy used to metabolize substrates above and beyond the requirements of intestinal tract mobility and absorption [3]. While there are several modulators of REE, and overall EE, the focus of this review will be on thyroid hormone (TH) and its mechanisms of action, on mitochondria. T4 is converted into T3 by deiodinase enzymes [5,6], which allow for time- and tissue-specific pre-receptor modulation of the hormonal signal. This review will discuss the developments in knowledge in this area, regarding TH’s role in modulating EE
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