scholarly journals Thyroid hormone signaling in energy homeostasis and energy metabolism

2014 ◽  
Vol 1311 (1) ◽  
pp. 77-87 ◽  
Author(s):  
Elizabeth A. McAninch ◽  
Antonio C. Bianco
Keyword(s):  
Energy Metabolism ◽  
Thyroid Hormone ◽  
Energy Homeostasis ◽  
Hormone Signaling

scholarly journals Absence of Thyroid Hormone Activation during Development Underlies a Permanent Defect in Adaptive Thermogenesis

2010 ◽  
Vol 31 (4) ◽  
pp. 603-603
Author(s):  
Jessica A. Hall ◽  
Scott Ribich ◽  
Marcelo A. Christoffolete ◽  
Gordana Simovic ◽  
Mayrin Correa-Medina ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Energy Homeostasis ◽  
Cell Model ◽  
Oxidative Capacity ◽  
Normal Serum ◽  
Hormone Signaling ◽  
Expression Of Genes ◽  
Brown Adipose ◽  
Serum T3 ◽  
A Cell

Abstract Type 2 deiodinase (D2), which is highly expressed in brown adipose tissue (BAT), is an enzyme that amplifies thyroid hormone signaling in individual cells. Mice with inactivation of the D2 pathway (D2KO) exhibit dramatically impaired thermogenesis in BAT, leading to hypothermia during cold exposure and a greater susceptibility to diet-induced obesity. This was interpreted as a result of defective acute activation of BAT D2. Here we report that the adult D2KO BAT has a permanent thermogenic defect that stems from impaired embryonic BAT development. D2KO embryos have normal serum T3 but due to lack of D2-generated T3 in BAT, this tissue exhibits decreased expression of genes defining BAT identity [i.e. UCP1, PGC-1α and Dio2 (nonfunctional)], which results in impaired differentiation and oxidative capacity. Coinciding with a reduction of these T3-responsive genes, there is oxidative stress that in a cell model of brown adipogenesis can be linked to decreased insulin signaling and decreased adipogenesis. This discovery highlights the importance of deiodinase-controlled thyroid hormone signaling in BAT development, where it has important metabolic repercussions for energy homeostasis in adulthood.

scholarly journals Oligodendroglial Energy Metabolism and (re)Myelination

Life ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 238
Author(s):  
Vanja Tepavčević
Keyword(s):  
Energy Metabolism ◽  
Alternative Energy ◽  
Energy Homeostasis ◽  
Energy Deficit ◽  
Maturation Stage ◽  
Trophic Support ◽  
Important Contributor ◽  
Alternative Energy Sources ◽  
Axonal Pathology ◽  
Sufficient Energy

Central nervous system (CNS) myelin has a crucial role in accelerating the propagation of action potentials and providing trophic support to the axons. Defective myelination and lack of myelin regeneration following demyelination can both lead to axonal pathology and neurodegeneration. Energy deficit has been evoked as an important contributor to various CNS disorders, including multiple sclerosis (MS). Thus, dysregulation of energy homeostasis in oligodendroglia may be an important contributor to myelin dysfunction and lack of repair observed in the disease. This article will focus on energy metabolism pathways in oligodendroglial cells and highlight differences dependent on the maturation stage of the cell. In addition, it will emphasize that the use of alternative energy sources by oligodendroglia may be required to save glucose for functions that cannot be fulfilled by other metabolites, thus ensuring sufficient energy input for both myelin synthesis and trophic support to the axons. Finally, it will point out that neuropathological findings in a subtype of MS lesions likely reflect defective oligodendroglial energy homeostasis in the disease.

scholarly journals Altered regulation of energy homeostasis in older rats in response to thyroid hormone administration

2013 ◽  
Vol 28 (3) ◽  
pp. 1499-1510 ◽  
Author(s):  
Stephane Walrand ◽  
Kevin R. Short ◽  
Lydia A. Heemstra ◽  
Colleen M. Novak ◽  
James A. Levine ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Energy Homeostasis ◽  
Hormone Administration ◽  
Altered Regulation

scholarly journals Thyroid Hormone Signaling in the Mouse Retina

PLoS ONE ◽  
2016 ◽  
Vol 11 (12) ◽  
pp. e0168003 ◽  
Author(s):  
Patrick Arbogast ◽  
Frédéric Flamant ◽  
Pierre Godement ◽  
Martin Glösmann ◽  
Leo Peichl
Keyword(s):  
Thyroid Hormone ◽  
Mouse Retina ◽  
Hormone Signaling

Glycogenic induction of thyroid hormone conversion and leptin system activation in the liver of postpartum dairy cows

2009 ◽  
Vol 57 (1) ◽  
pp. 139-146
Author(s):  
Andrea Győrffy ◽  
Mónika Keresztes ◽  
Vera Faigl ◽  
Vilmos Frenyó ◽  
Margit Kulcsár ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Energy Balance ◽  
Dairy Cows ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Energy Content ◽  
Short Form ◽  
Negative Energy ◽  
Type I ◽  
Leptin System

In the regulation of energy metabolism, the liver plays an important role in the reinforcement of energy production. In periparturient cows the energy homeostasis turns into a negative energy balance that may shift the physiological regulation of energy balance towards pathological processes. Propylene glycol (PG), as a complementary source of energy used in the nutrition of dairy cows, alters systemic thyroid hormone economy; however, the exact mechanism through which highly glycogenic feed supplements impact liver metabolism is little known. Previous studies showed that only leptin receptors are expressed in the liver of cows, and now we report that leptin mRNA is expressed in the liver of cows as well. The present results show that the mRNA of leptin and its receptors are differentially modulated by the increased energy content of the feed consumed. Simultaneous changes in hepatic type I deiodinase activity suggest that hepatic modulation of the leptin system by PG supplementation may be mediated by an increased local thyroxine-triiodothyronine conversion. Since PG supplementation with simultaneous T4–T3 turnover and increased hepatic leptin- and short-form leptin receptor mRNA were not associated with a significant change in hepatic total lipid levels, it is suggested that the leptin system, directly or indirectly modulated by thyroid hormones, may represent a local defence mechanism to prevent fatty liver formation.

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