1. Temperature homeostasis in mice lacking the p43 mitochondrial T3 receptor.
- Author
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Bertrand-Gaday C, Pessemesse L, Cabello G, Wrutniak-Cabello C, and Casas F
- Subjects
- Adipose Tissue, Brown pathology, Animals, Basal Metabolism, Cold Temperature adverse effects, DNA Copy Number Variations, DNA, Mitochondrial metabolism, Energy Intake, Gene Expression Regulation, Hyperphagia etiology, Hyperphagia pathology, Male, Mice, Inbred C57BL, Mice, Knockout, Thermogenesis, Thyroid Hormone Receptors alpha genetics, Adaptation, Physiological, Adipose Tissue, Brown metabolism, Body Temperature Regulation, Energy Metabolism, Hyperphagia metabolism, Mitochondria metabolism, Thyroid Hormone Receptors alpha metabolism
- Abstract
Thyroid hormones and Thra gene play a key role in energy expenditure regulation, temperature homeostasis, and mitochondrial function. To decipher the function of the mitochondrial TRα receptor in these phenomena, we used mice lacking specifically the p43 mitochondrial T3 receptor. We found that these animals were hypermetabolic, hyperphagic, and displayed a down setting of the core body temperature. However, p43-/- animals do not present cold intolerance or defect of facultative thermogenesis. In addition, the mitochondrial function of BAT is slightly affected in the absence of p43. Our study, therefore, suggests a complementarity of action between the mitochondrial receptor and other proteins encoded by the Thra gene in the control of basal metabolism, facultative thermogenesis, and determination of the set point of temperature regulation., (© 2016 Federation of European Biochemical Societies.)
- Published
- 2016
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