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Am J Physiol Endocrinol Metab (July 30, 2002). doi:10.1152/ajpendo.00196.2002
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Articles in PresS, published online ahead of print July 30, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00196.2002
Submitted on May 7, 2002
Accepted on July 10, 2002

Central stimulatory effect of leptin on T3 production is mediated by brown adipose tissue type 2 deiodinase

Philippe Cettour-Rose1, Albert G Burger1, Christophe A Meier1, Theodore J Visser2, and Francoise Rohner-Jeanrenaud1*

1 Division of Endocrinology and Diabetology, Department of Medicine, University of Geneva, Geneva, Switzerland
2 Department of Internal Medicine III, Erasmus University, Rotterdam, Netherlands

* To whom correspondence should be addressed. E-mail: f.rohner-jeanrenaud{at}hcuge.ch.

To assess whether intracerebroventricular (i.c.v.) leptin administration affects monodeiodinase type 2 (D2) activity in the tissues where it is expressed (i.e. cerebral cortex, hypothalamus, pituitary, and brown adipose tissue, BAT), hepatic monodeiodinase type 1 (D1) activity was inhibited with propylthiouracil (PTU) and small doses of T4 (0.6 nmol/100g bw/d) were supplemented to compensate for the PTU-induced hypothyroidism. Two groups of rats were i.c.v. infused with leptin for 6 days, one of them being additionally treated with rT3, an inhibitor of D2. Control rats were i.c.v. infused with vehicle, and pair-fed to the amount of food consumed by leptin-infused animals. I.c.v. leptin administration produced marked increases in D2 mRNA expression and activity in BAT, changes that were likely responsible for increased plasma T3 and decreased plasma T4 levels. Indeed, plasma T3 and T4 concentrations were unaltered by i.c.v. leptin administration in the presence of rT3. The additional observation of a leptin-induced increased mRNA expression of BAT uncoupling protein-1 suggested that the effect on BAT D2 may be mediated by the sympathetic nervous system.




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