Fatty acid metabolism and thyroid hormones.
The importance of thyroid hormone signaling in the acute regulation of metabolic activity has been recognized for decades. Slowly, the underlying mechanisms responsible for this activity are being elucidated. A prominent characteristic of thyroid signaling is rapid increases in oxygen consumption and ATP production. This discovery implicated a non-genomic regulation of mitochondrial metabolism by thyroid hormones. Another important clue came from the discovery that thyroid hormones stimulated fatty acid oxidation (FAO) in a variety of tissues in a receptor-dependent, but transcriptional-independent manner. Recently, key linkages between thyroid hormone signaling and specific mitochondrial-targeted pathways have been discovered. This review focuses on the molecular mechanisms by which mitochondrial FAO can be increased through thyroid hormone signaling. The roles of both the full-length and shortened mitochondrial isoforms of thyroid hormone receptor will be discussed. Additionally, the impact of thyroid hormone signaling on dyslipidemias such as obesity, type II diabetes, and fatty liver disease will be considered.
Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, South Texas Research Facility Neuroscience Center, 8403 Floyd Curl Drive, San Antonio, TX 78229-3904, USA.
Naomi L
NL
Sayre
Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, South Texas Research Facility Neuroscience Center, 8403 Floyd Curl Drive, San Antonio, TX 78229-3904, USA.
James D
JD
Lechleiter
3,3,5 triiodothyronine; ACC; AMPK; CO23; CPT; GC-1; LCHAD; MB07344; MTP; T2; T3,3,5 diiodothyroinine; TRα; TRβ; acetyl-coA carboxylase; adenosine monophosphate activated protein-kinase; c-erbA; carnitine palmitoyl transferase; dyslipidemia; energy homeostasis; fatty acid; fatty acid oxidation; fatty acid trafficking; insulin resistance; long-chain acyl CoA dehydrogenase; metabolic syndrome; mitochondria; mitochondrial trifunctional protein; non-alcoholic fatty liver disease; non-genomic; obesity; p28; p30; p43; steatosis; thyroid hormone; thyroid hormone analogs; thyroid hormone receptor; thyrotoxicity; type II diabetes