Endocrine Abstracts

A normal thyroid status is crucial for normal tissue and organ functioning, including temperature homeostasis. The tissue-specific actions of TH on body temperature regulation and thermogenesis are largely modulated via thyroid hormone receptor TRα. Consequently, mice expressing a mutant TRα display bradycardia and a reduced body temperature at 22°C ambient temperature due to excessive heat loss via the tail. To test whether this peripheral heat loss is the sole reason for the hypothermia, we housed TRα-mutants at 30°C, where tail heat loss is minimized. Using infrared thermography, we revealed that the heat loss effect via the tail could be reversed; however, body temperature surprisingly still remains lower during the inactive phase in TRα-mutants. The observed lack of a compensatory brown fat activation suggests that the central regulation of temperature homeostasis may be impaired in TRα-mutants indicating a lower central body temperature set-point, also at 30°C. Whether the expression of mutant TRα in the brain can indeed lower the central body temperature set-point will be tested in future experiments.