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Am J Physiol Endocrinol Metab 283: E496-E502, 2002. First published May 15, 2002; doi:10.1152/ajpendo.00540.2001
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Vol. 283, Issue 3, E496-E502, September 2002

Brown fat thermogenesis in cold-acclimated rats is not abolished by the suppression of thyroid function

Angel A. Zaninovich1, Marcela Raíces2, Inés Rebagliati1, Conrado Ricci1, and Karl Hagmüller1

1 Thyroid Research Laboratory, Nuclear Medicine Center, University Hospital, and 2 Institute of Genetic Engineering and Molecular Biology, University of Buenos Aires, 1120 Buenos Aires, Argentina

The effects of long-term cold exposure on brown adipose tissue (BAT) thermogenesis in hypothyroid rats have been examined. Thyroid ablation was performed in normal rats after 2 mo of exposure to 4°C, when BAT hypertrophy and thermogenic activity were maximal. After ablation, hypothyroid and normal controls remained in the cold for 2 additional months. At the end of the 4-mo cold exposure, all untreated hypothyroid rats were alive, had normal body temperature, and had gained an average 12.8% more weight than normal controls. Long-term cold exposure of hypothyroid rats markedly increased BAT weight, mitochondrial proteins, uncoupling protein (UCP)-1, mRNA for UCP-1, and oxygen consumption to levels similar to those seen in cold-exposed normal rats. The results indicate that thyroid hormones are required for increased thermogenic capacity to occur as an adaptation to long-term cold exposure. However, cold adaptation can be maintained in the absence of thyroid hormone.

cold acclimation; uncoupling protein-1; hypothyroidism; oxygen consumption; norepinephrine


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