In mice, the thyroid hormone T3 raises body temperature even when the thyroid hormone receptor TRα1 is not functional in skeletal muscle, indicating that the temperature increase does not depend on...
Mechanism
Synthesis from 1 study
T3 makes mice warmer even when their muscles can't respond to it, because the hormone works through other parts of the body — like the brain or liver — to generate heat, not the muscles or fat (10.1096/fj.202001258RR). This means the body has a backup way to raise temperature that doesn't rely on...
Most probable mechanism
When thyroid hormone T3 is present, it raises body temperature in mice even when the thyroid hormone receptor TRα1 is disabled in skeletal muscle, meaning the muscles aren't responsible for the heat. This happens because T3 acts elsewhere in the body — likely in the brain or other tissues — to increase heat production, without relying on brown fat or muscle to do it, as shown in mice that still get warmer despite lacking functional TRα1 in muscle (10.1096/fj.202001258RR).
T3 enters circulation and binds to thyroid hormone receptors in non-skeletal muscle tissues, such as the hypothalamus or liver, triggering downstream signaling that increases metabolic heat production.
This T3 signaling in non-muscle tissues elevates core body temperature independently of skeletal muscle TRα1, as demonstrated by identical hyperthermic responses in mice with and without functional TRα1 in muscle.
The hyperthermia is not mediated by brown adipose tissue (BAT), as no increase in UCP1 expression or BAT mass occurs in T3-treated mice lacking muscle TRα1.
T3-induced hyperthermia is dissociated from energy expenditure, which requires muscle TRα1, confirming that the thermogenic pathway for body temperature rise operates through a separate, non-muscle mechanism.
Evidence from Studies
Supporting (1)
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Thyroid hormone receptor α in skeletal muscle is essential for T3‐mediated increase in energy expenditure
Contradicting (0)
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