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Am J Physiol Endocrinol Metab (May 15, 2002). doi:10.1152/ajpendo.00540.2001
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Articles in PresS, published online ahead of print May 14, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00540.2001
Submitted on December 5, 2001
Accepted on May 13, 2002

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

Angel Zaninovich1, Marcela Raices2, Ines Rebagliati1*, Conrado Ricci1, and Karl Hagmuller1

1 Nuclear Medicine, Hospital de Clinicas, Buenos Aires, Buenos Aires, Argentina
2 Institute of Genetic Engineering and Molecular Biology, Buenos Aires, Buenos Aires, Argentina; Nuclear Medicine, Hospital de Clinicas, Buenos Aires, Buenos Aires, Argentina

* To whom correspondence should be addressed. E-mail: azaninovich{at}sinectis.com.ar.

The effects of long-term cold exposure on brown adipose tissue (BAT) thermogenesis in hypothyroid rats have been examined. The thyroid ablation was performed in normal rats after two months of exposure to 4°C, when BAT hyperthrophy and thermogenic activity were maximal. Following ablation, hypothyroid and normal controls remained in the cold for 2 additional months. At the end of 4-month cold exposure, all untreated hypothyroid rats were alive, had normal body temperature and gained an average 12.8% more weight that normal controls. Long-term cold exposure of hypothyroid rats markedly increased BAT weight, mitochondrial proteins, UCP1, mRNA for UCP1 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.




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