Abstract
The paper by Heemstra et al. (1) in this issue of JCEM provides some striking and unexpected results that have significant implications for our understanding of thyroid hormone physiology in humans. Their findings help to clarify how the regulation of type 2 iodothyronine deiodinase (D2) in skeletal muscle is affected by thyroid status, fasting, and insulin, and illustrate the importance of its functional activity in that tissue. They also contribute to our understanding of the effects of illness and hypothyroidism on thyroid hormone metabolism and help define the role of skeletal muscle D2 in the production of the active hormone T3.
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