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Central Hypothyroidism Impairs Heart Rate Stability and Prevents Thyroid Hormone-Induced Cardiac Hypertrophy and Pyrexia. | LitMetric

Central Hypothyroidism Impairs Heart Rate Stability and Prevents Thyroid Hormone-Induced Cardiac Hypertrophy and Pyrexia.

Thyroid

Department of Molecular Endocrinology, Institute for Endocrinology and Diabetes, Center of Brain Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.

Published: August 2020

AI Article Synopsis

  • Tachycardia, cardiac hypertrophy, and elevated body temperature are key indicators of systemic hyperthyroidism, attributed to excessive thyroid hormone action in tissues, but new findings suggest significant contributions from the brain as well.
  • A study using mice that lack specific thyroid hormone transporters (double knock-out) compared their body temperature and heart function to wild-type mice treated with thyroid hormone, revealing that central thyroid hormone actions are crucial for symptoms like hyperthermia and cardiac hypertrophy.
  • The results indicate that while heart rate remained generally stable in both models, the double knock-out mice showed irregularities in heart rate patterns, highlighting the importance of the central nervous system in managing these cardiovascular issues.

Article Abstract

Tachycardia, cardiac hypertrophy, and elevated body temperature are major signs of systemic hyperthyroidism, which are considered to reflect the excessive thyroid hormone (TH) action in the respective peripheral tissues. However, recent observations indicate that the central actions of TH also contribute substantially to cardiovascular regulation and thermogenesis. In this study, we dissect the individual contributions of peripheral TH action versus the central effects in body temperature regulation and cardiovascular functions by taking advantage of mice lacking the TH transporters monocarboxylate transporter 8 (MCT8) and organic anion transporting polypeptide 1C1 (OATP1C1) ( double knock-out [dko]), which exhibit elevated serum triiodothyronine (T3) levels while their brain is in a profoundly hypothyroid state. We compared these animals with wild-type (WT) mice that were treated orally with T3 to achieve similarly elevated serum T3 levels, but are centrally hyperthyroid. For the studies, we used radiotelemetry, infrared thermography, gene expression profiling, Western blot analyses, and enzyme linked immunosorbent assays (ELISA) assays. Our analyses revealed mild hyperthermia and cardiac hypertrophy in T3-treated WT mice but not in dko animals, suggesting that central actions of TH are required for these hyperthyroid phenotypes. Although the average heart rate was unaffected in either model, the dko exhibited an altered heart rate frequency distribution with tachycardic bursts in active periods and bradycardic episodes during resting time, demonstrating that the stabilization of heart rate by the autonomic nervous system can be impaired in centrally hypothyroid animals. Our studies unravel distinct phenotypical traits of hyperthyroidism that depend on an intact central nervous system, and provide valuable insight into the cardiovascular pathology of the Allan-Herndon-Dudley syndrome, a condition caused by the lack of MCT8 in humans.

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Source
http://dx.doi.org/10.1089/thy.2019.0705DOI Listing

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