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Submitted on April 28, 2004
Accepted on July 26, 2004
Department of Metabolic Medicine, Imperial College Faculty of Medicine at Hammersmith Campus, Du Cane Road, London, W12 0NN, U.K.; Department of Physiology, St George's Hospital Medical School, University of London, SW17 0RE, U.K.; Department of Mathematics, Statistics Group, Imperial College, South Kensington Campus, London. SW7 3AZ, U.K.
* To whom correspondence should be addressed. E-mail: s.bloom{at}imperial.ac.uk.
Increased food intake is characteristic of hyperthyroidism, although this is presumed to compensate for a state of negative energy balance. However, here we show that the thyroid hormone tri-iodothyronine (T3) directly stimulates feeding at the level of the hypothalamus. Peripheral administration of T3 doubled food intake in ad libitum fed rats over 2 h and induced expression of the immediate early gene, Egr-1, in the hypothalamic ventromedial nucleus (VMN), while maintaining plasma fT3 levels within the normal range. T3-induced feeding occurred without altering energy expenditure or locomotion. Injection of T3 directly into the VMN produced a 4-fold increase in food intake in the first hour. The majority of T3 in the brain is reported to be produced by tissue-specific conversion of T4 to T3 by the enzyme type 2 iodothyronine deiodinase (D2). Hypothalamic D2 mRNA expression showed a diurnal variation, with a peak in the nocturnal feeding phase. Hypothalamic D2 mRNA levels also increased following a 12- and 24 h fast, suggesting that local production of T3 may play a role in this T3 feeding circuit. Thus, we propose a novel hypothalamic feeding circuit in which T3, from the peripheral circulation or produced by local conversion, stimulates food intake via the VMN.
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