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| The EMBO Journal
(1998) 17, 455–461, doi:10.1093/emboj/17.2.455 |
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Abnormal heart rate and body temperature in mice lacking thyroid hormone receptor  1 |
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| Lilian Wikström1, Catarina Johansson2, Carmen Saltó1, 6, Carrolee Barlow1, 3, 6, Angel Campos Barros4, Frank Baas5, Douglas Forrest4, Peter Thorén2 and Björn Vennström1 |
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1 Department of Cell and Molecular Biology, Karolinska Institute, S-17177 Stockholm, Sweden 2 Department of Physiology, Karolinska Institute, S-17177 Stockholm, Sweden 3 Laboratory of Genetic Disease Research, NIH, Building 49/4A67, Bethesda, MD 20892-4470, USA 4 Department of Human Genetics, Mount Sinai School of Medicine, New York, NY 10029, USA 5 Department of Neurology, Academic Medical Center, University of Amsterdam, The Netherlands 6 C.Saltó and C.Barlow contributed equally to this work To whom correspondence should be addressed Björn Vennström, bjorn.vennstrom@cmb.ki.se Received 24 March 1997; Revised 28 October 1997; Accepted 29 October 1997. |
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| Abstract |
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| Thyroid hormone, acting through several nuclear hormone receptors, plays important roles in thermogenesis, lipogenesis and maturation of the neonatal brain. The receptor specificity for mediating these effects is largely unknown, and to determine this we developed mice lacking the thyroid hormone receptor TR1. The mice have an average heart rate 20% lower than that of control animals, both under normal conditions and after thyroid hormone stimulation. Electrocardiograms show that the mice also have prolonged QRS- and QTend-durations. The mice have a body temperature 0.5°C lower than normal and exhibit a mild hypothyroidism, whereas their overall behavior and reproduction are normal. The results identify specific and important roles for TR1 in regulation of tightly controlled physiological functions, such as cardiac pacemaking, ventricular repolarisation and control of body temperature. |
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| Keywords: bradycardia, hypothermia, thyroid hormone |
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