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Related Experiment Video

Updated: May 25, 2026

A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function

A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function

Published on: October 6, 2023

Hypothalamic mTOR pathway mediates thyroid hormone-induced hyperphagia in hyperthyroidism.

Luis Varela¹, Noelia Martínez-Sánchez, Rosalía Gallego

¹Department of Physiology, School of Medicine-CIMUS, University of Santiago de Compostela, Instituto de Investigación Sanitaria, Santiago de Compostela (A Coruña) 15782, Spain.

The Journal of Pathology

|February 2, 2012

Summary

This summary is machine-generated.

Hyperthyroidism increases appetite by activating the mammalian target of rapamycin (mTOR) pathway in the hypothalamus. Inhibiting mTOR signaling in hyperthyroid rats reversed overeating and promoted weight loss.

Related Experiment Videos

Last Updated: May 25, 2026

A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function

A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function

Published on: October 6, 2023

Area of Science:

Neuroendocrinology
Metabolic Regulation

Background:

Hyperthyroidism causes increased energy expenditure and overeating (hyperphagia) in rats.
Central mechanisms of hyperthyroidism-induced hyperphagia are not fully understood, though hypothalamic AMPK and fatty acid metabolism are implicated.

Purpose of the Study:

To investigate the role of hypothalamic mammalian target of rapamycin (mTOR) signaling in mediating hyperphagia during hyperthyroidism.
To explore the relationship between thyroid hormone signaling, neuropeptide expression, and feeding behavior in the hypothalamus.

Main Methods:

Examined hypothalamic mTOR signaling, neuropeptide mRNA levels (AgRP, NPY, POMC), and feeding behavior in hyperthyroid rats.
Administered thyroid hormone (T3) centrally or genetically activated thyroid hormone signaling in the arcuate nucleus (ARC).
Inhibited mTOR signaling using rapamycin in hyperthyroid rats.

Main Results:

Hyperthyroid rats showed upregulated hypothalamic mTOR signaling, increased AgRP and NPY mRNA, and decreased POMC mRNA in the ARC.
Central T3 administration or ARC thyroid hormone signaling activation mimicked hyperthyroidism effects on feeding and mTOR.
Rapamycin treatment reversed hyperphagia, normalized neuropeptide expression, and caused weight loss in hyperthyroid rats.

Conclusions:

Thyroid hormone-induced upregulation of hypothalamic mTOR signaling contributes to hyperphagia in hyperthyroidism.
Targeting mTOR signaling offers a potential therapeutic strategy for managing metabolic disturbances associated with hyperthyroidism.