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Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide
Published on: May 12, 2023
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Fatty acid metabolism and thyroid hormones
Naomi L Sayre1, James D Lechleiter1
1Department 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.
Current Trends in Endocrinology
|January 18, 2014
Summary
Thyroid hormones rapidly boost metabolism and ATP production through non-genomic mitochondrial pathways. This review explores how thyroid hormone signaling enhances fatty acid oxidation and impacts metabolic diseases.
Area of Science:
- Biochemistry
- Molecular Biology
- Endocrinology
Background:
- Thyroid hormone signaling is crucial for acute metabolic regulation.
- Thyroid hormones rapidly increase oxygen consumption and ATP production.
- This suggests non-genomic regulation of mitochondrial metabolism.
Purpose of the Study:
- To review the molecular mechanisms of thyroid hormone-induced mitochondrial fatty acid oxidation (FAO).
- To discuss the roles of full-length and mitochondrial thyroid hormone receptors.
- To examine the impact on dyslipidemias like obesity, type II diabetes, and fatty liver disease.
Main Methods:
- Review of existing literature on thyroid hormone signaling and mitochondrial metabolism.
- Focus on receptor-dependent, transcriptional-independent mechanisms.
- Analysis of molecular pathways linking thyroid hormones to FAO.
Main Results:
- Thyroid hormones stimulate FAO via receptor-dependent, transcriptional-independent pathways.
- Specific mitochondrial-targeted pathways are linked to thyroid hormone signaling.
- Both full-length and shortened mitochondrial thyroid hormone receptors play roles.
Conclusions:
- Thyroid hormone signaling directly enhances mitochondrial fatty acid oxidation.
- Understanding these mechanisms is key to addressing metabolic diseases.
- Further research into thyroid hormone's role in dyslipidemias is warranted.
Keywords:
3,3,5 triiodothyronineACCAMPKCO23CPTGC-1LCHADMB07344MTPT2T3,3,5 diiodothyroinineTRαTRβacetyl-coA carboxylaseadenosine monophosphate activated protein-kinasec-erbAcarnitine palmitoyl transferasedyslipidemiaenergy homeostasisfatty acidfatty acid oxidationfatty acid traffickinginsulin resistancelong-chain acyl CoA dehydrogenasemetabolic syndromemitochondriamitochondrial trifunctional proteinnon-alcoholic fatty liver diseasenon-genomicobesityp28p30p43steatosisthyroid hormonethyroid hormone analogsthyroid hormone receptorthyrotoxicitytype II diabetes
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