Thyroid Hormone Regulation of Metabolism
2014/04/01 by Rashmi Mullur, Yan-Yun Liu, Yan‐Yun Liu +1 · 2,386 citations
Medicine · Neuroscience · #Adipose tissue #Biochemistry #Biology #Brown adipose tissue #Cell biology #Deiodinase #Endocrinology #Growth Hormone and Insulin-like Growth Factors #Hormone #Hormone receptor #Internal medicine #Lipid metabolism #Medicine #Nuclear receptor #Regulation of Appetite and Obesity #Signal transduction #Thyroid #Thyroid Disorders and Treatments #Thyroid hormone receptor #Thyroid hormone receptor beta #Transcription factor #Triiodothyronine
paper · doi:10.1152/physrev.00030.2013
published in Physiological Reviews 94(2), 355-382 (American Physiological Society)
openalex publication_date 2014/04/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/06
Abstract
Thyroid hormone (TH) is required for normal development as well as regulating metabolism in the adult. The thyroid hormone receptor (TR) isoforms, α and β, are differentially expressed in tissues and have distinct roles in TH signaling. Local activation of thyroxine (T4), to the active form, triiodothyronine (T3), by 5'-deiodinase type 2 (D2) is a key mechanism of TH regulation of metabolism. D2 is expressed in the hypothalamus, white fat, brown adipose tissue (BAT), and skeletal muscle and is required for adaptive thermogenesis. The thyroid gland is regulated by thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH). In addition to TRH/TSH regulation by TH feedback, there is central modulation by nutritional signals, such as leptin, as well as peptides regulating appetite. The nutrient status of the cell provides feedback on TH signaling pathways through epigentic modification of histones. Integration of TH signaling with the adrenergic nervous system occurs peripherally, in liver, white fat, and BAT, but also centrally, in the hypothalamus. TR regulates cholesterol and carbohydrate metabolism through direct actions on gene expression as well as cross-talk with other nuclear receptors, including peroxisome proliferator-activated receptor (PPAR), liver X receptor (LXR), and bile acid signaling pathways. TH modulates hepatic insulin sensitivity, especially important for the suppression of hepatic gluconeogenesis. The role of TH in regulating metabolic pathways has led to several new therapeutic targets for metabolic disorders. Understanding the mechanisms and interactions of the various TH signaling pathways in metabolism will improve our likelihood of identifying effective and selective targets.
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