ArticleEuropean thyroid journal2026
Triiodothyroacetic acid exerts tissue-specific thyromimetic effects without tachycardia and hyperthermia in male mice.
Article in European thyroid journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThyroid hormones regulate cardiovascular functions and energy homeostasis, including thermogenesis, through binding to nuclear thyroid hormone receptors. The thyroid hormone analog 3,3',5-triiodothyroacetic acid (TRIAC) has recently emerged as a therapeutic candidate for thyroid hormone transporter deficiencies (Allan-Herndon-Dudley syndrome) or thyroid hormone resistance β. Although TRIAC shows promise for these conditions, a comprehensive characterization focusing on heart and body temperature regulation has not been systematically performed in mice.
methodsAs this knowledge is critical for determining its safety profile and therapeutic advantages over conventional thyroid hormone therapy, we administered TRIAC to wild-type mice for 14 days and assessed molecular (real-time PCR, western blot, and immunoassays) and physiological (infrared thermography and blood pressure) responses.
resultsTRIAC treatment reduced circulating thyroxine levels and induced robust upregulation of hepatic thyroid hormone-responsive genes, including Dio1 and Me1, demonstrating classical thyromimetic activity. However, cardiovascular analysis revealed normal blood pressure and heart rate, and there were no signs of cardiac hypertrophy despite specific molecular changes in cardiac gene expression. At the metabolic level, we surprisingly did not observe any effect on brown fat thermogenesis or body temperature, while in muscle, Ucp3 and Gpd2 were reduced.
conclusionTaken together, our comparative in vivo analysis demonstrates variable TRIAC responsiveness across tissues. Under defined conditions, the drug produces defined metabolic responses while avoiding classical hyperthyroid manifestations, such as tachycardia or hyperthermia, thus supporting its potential therapeutic use in thyroid hormone resistance conditions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.