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Regulation of skeletal muscle mitochondrial activity by thyroid hormones: focus on the "old" triiodothyronine and the "emerging" 3,5-diiodothyronine.

Lombardi A, Moreno M, de Lange P, Iossa S, Busiello RA, Goglia F - Front Physiol (2015)

Bottom Line: Among these, 3,5-diiodo-L-thyronine (T2) affects energy metabolism, SKM substrate utilization, and mitochondrial functionality.The effects it exerts on SKM mitochondria involve more aspects of mitochondrial bioenergetics; among these, respiratory chain activity, mitochondrial thermogenesis, and lipid-handling are stimulated rapidly.This mini review focuses on signaling and biochemical pathways activated by T3 and T2 in SKM that influence the above processes.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of Naples Federico II Naples, Italy.

ABSTRACT
3,5,3'-Triiodo-L-thyronine (T3) plays a crucial role in regulating metabolic rate and fuel oxidation; however, the mechanisms by which it affects whole-body energy metabolism are still not completely understood. Skeletal muscle (SKM) plays a relevant role in energy metabolism and responds to thyroid state by remodeling the metabolic characteristics and cytoarchitecture of myocytes. These processes are coordinated with changes in mitochondrial content, bioenergetics, substrate oxidation rate, and oxidative phosphorylation efficiency. Recent data indicate that "emerging" iodothyronines have biological activity. Among these, 3,5-diiodo-L-thyronine (T2) affects energy metabolism, SKM substrate utilization, and mitochondrial functionality. The effects it exerts on SKM mitochondria involve more aspects of mitochondrial bioenergetics; among these, respiratory chain activity, mitochondrial thermogenesis, and lipid-handling are stimulated rapidly. This mini review focuses on signaling and biochemical pathways activated by T3 and T2 in SKM that influence the above processes. These novel aspects of thyroid physiology could reveal new perspectives for understanding the involvement of SKM mitochondria in hypo- and hyper-thyroidism.

No MeSH data available.


Related in: MedlinePlus

Schematic representation of the coordinated events activated by T3 that take place in both nuclei and mitochondria, promoting mitochondrial biogenesis. T3 directly activates the transcription of nuclear- and mitochondrial-genes coding for component of respiratory chain by binding to its nuclear TRs and mitochondrial p43. T3 also indirectly activates respiratory genes transcription by up-regulating the transcription of intermediate factors (such as NRF-1 and -2 and PGC1a). AMPK activation also mediates an indirect effect of T3 on mitochondrial biogenesis.
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Figure 1: Schematic representation of the coordinated events activated by T3 that take place in both nuclei and mitochondria, promoting mitochondrial biogenesis. T3 directly activates the transcription of nuclear- and mitochondrial-genes coding for component of respiratory chain by binding to its nuclear TRs and mitochondrial p43. T3 also indirectly activates respiratory genes transcription by up-regulating the transcription of intermediate factors (such as NRF-1 and -2 and PGC1a). AMPK activation also mediates an indirect effect of T3 on mitochondrial biogenesis.

Mentions: T3 positively regulates the expression of intermediate factors, such as nuclear respiratory factors (NRF)-1 and -2, which enhance the expression of mitochondrial transcription factor-A, a nuclear-encoded transcription factor essential for replication, maintenance, and transcription of mitochondrial DNA. T3 also controls the expression of coactivator of peroxisome proliferator activated receptor γ (PPARγ) PGC-1α (Weitzel et al., 2001), a central regulator of mitochondrial gene expression and biogenesis (Puigserver, 2005). PGC-1α regulates gene expression through its interactions with DNA-bound transcription factors, including TR, PPAR, and NRF-1 (Knutti and Kralli, 2001, Figure 1).


Regulation of skeletal muscle mitochondrial activity by thyroid hormones: focus on the "old" triiodothyronine and the "emerging" 3,5-diiodothyronine.

Lombardi A, Moreno M, de Lange P, Iossa S, Busiello RA, Goglia F - Front Physiol (2015)

Schematic representation of the coordinated events activated by T3 that take place in both nuclei and mitochondria, promoting mitochondrial biogenesis. T3 directly activates the transcription of nuclear- and mitochondrial-genes coding for component of respiratory chain by binding to its nuclear TRs and mitochondrial p43. T3 also indirectly activates respiratory genes transcription by up-regulating the transcription of intermediate factors (such as NRF-1 and -2 and PGC1a). AMPK activation also mediates an indirect effect of T3 on mitochondrial biogenesis.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4543916&req=5

Figure 1: Schematic representation of the coordinated events activated by T3 that take place in both nuclei and mitochondria, promoting mitochondrial biogenesis. T3 directly activates the transcription of nuclear- and mitochondrial-genes coding for component of respiratory chain by binding to its nuclear TRs and mitochondrial p43. T3 also indirectly activates respiratory genes transcription by up-regulating the transcription of intermediate factors (such as NRF-1 and -2 and PGC1a). AMPK activation also mediates an indirect effect of T3 on mitochondrial biogenesis.
Mentions: T3 positively regulates the expression of intermediate factors, such as nuclear respiratory factors (NRF)-1 and -2, which enhance the expression of mitochondrial transcription factor-A, a nuclear-encoded transcription factor essential for replication, maintenance, and transcription of mitochondrial DNA. T3 also controls the expression of coactivator of peroxisome proliferator activated receptor γ (PPARγ) PGC-1α (Weitzel et al., 2001), a central regulator of mitochondrial gene expression and biogenesis (Puigserver, 2005). PGC-1α regulates gene expression through its interactions with DNA-bound transcription factors, including TR, PPAR, and NRF-1 (Knutti and Kralli, 2001, Figure 1).

Bottom Line: Among these, 3,5-diiodo-L-thyronine (T2) affects energy metabolism, SKM substrate utilization, and mitochondrial functionality.The effects it exerts on SKM mitochondria involve more aspects of mitochondrial bioenergetics; among these, respiratory chain activity, mitochondrial thermogenesis, and lipid-handling are stimulated rapidly.This mini review focuses on signaling and biochemical pathways activated by T3 and T2 in SKM that influence the above processes.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of Naples Federico II Naples, Italy.

ABSTRACT
3,5,3'-Triiodo-L-thyronine (T3) plays a crucial role in regulating metabolic rate and fuel oxidation; however, the mechanisms by which it affects whole-body energy metabolism are still not completely understood. Skeletal muscle (SKM) plays a relevant role in energy metabolism and responds to thyroid state by remodeling the metabolic characteristics and cytoarchitecture of myocytes. These processes are coordinated with changes in mitochondrial content, bioenergetics, substrate oxidation rate, and oxidative phosphorylation efficiency. Recent data indicate that "emerging" iodothyronines have biological activity. Among these, 3,5-diiodo-L-thyronine (T2) affects energy metabolism, SKM substrate utilization, and mitochondrial functionality. The effects it exerts on SKM mitochondria involve more aspects of mitochondrial bioenergetics; among these, respiratory chain activity, mitochondrial thermogenesis, and lipid-handling are stimulated rapidly. This mini review focuses on signaling and biochemical pathways activated by T3 and T2 in SKM that influence the above processes. These novel aspects of thyroid physiology could reveal new perspectives for understanding the involvement of SKM mitochondria in hypo- and hyper-thyroidism.

No MeSH data available.


Related in: MedlinePlus