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The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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Coupling between Nutrient Availability and Thyroid Hormone Activation.

Lattoya J Lartey1, João Pedro Werneck-de-Castro2, InSug O-Sullivan3

  • 1From the Department of Molecular and Cellular Pharmacology, University of Miami, Miller School of Medicine, Miami, Florida 33136.

The Journal of Biological Chemistry
|October 27, 2015
PubMed
Summary

Food availability stimulates thyroid hormone activation by increasing type 2 deiodinase (DIO2) expression in muscle. This occurs through the PI3K-mTORC2-Akt pathway, which relieves FOXO1-mediated repression of DIO2 during nutrient abundance.

Keywords:
FOXO1insulinmTOR complex (mTORC)signal transductionsignalingthyroid hormonetype 2 deiodinase

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolism

Background:

  • Thyroid hormones regulate metabolism, and their activity is influenced by nutrient availability.
  • Leptin signaling, triggered by food intake, upregulates thyrotropin-releasing hormone and thyroid-stimulating hormone.
  • The conversion of thyroxine (T4) to the active triiodothyronine (T3) is a critical regulatory step.

Purpose of the Study:

  • To investigate how food availability influences thyroid hormone activation at the tissue level.
  • To elucidate the molecular mechanisms regulating type 2 deiodinase (DIO2) expression in response to nutrients.
  • To identify key signaling pathways involved in nutrient-sensing for thyroid hormone metabolism.

Main Methods:

  • Utilized a cell model transitioning from low (0.1%) to high (10%) fetal bovine serum (FBS) to mimic fasting and feeding states.
  • Employed rictor knockdown to define the role of the mTORC2 pathway.
  • Used FOXO1 inhibition, constitutively active FOXO1, and ChIP assays to study DIO2 promoter regulation.
  • Investigated the role of insulin signaling in FOXO1 knockout mice.

Main Results:

  • Food availability (10% FBS) accelerates T4 to T3 conversion in mouse skeletal muscle via DIO2.
  • DIO2 expression is transcriptionally repressed by FOXO1 binding to its promoter during low nutrient conditions (0.1% FBS).
  • Nutritional stimulation (10% FBS) leads to decreased FOXO1 binding and activation of the DIO2 promoter, mediated by the PI3K-mTORC2-Akt pathway.
  • Insulin acts as a key signaling molecule in this nutrient-sensing pathway.

Conclusions:

  • FOXO1 acts as a repressor of DIO2 during fasting conditions.
  • Nutritional cues activate the PI3K-mTORC2-Akt pathway, leading to the derepression of DIO2 and enhanced thyroid hormone activation.
  • This mechanism highlights a direct link between nutrient status and thyroid hormone metabolism in skeletal muscle.