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Submitted on October 15, 2004
Accepted on January 6, 2005
Department of Obstetrics and Gynecology and Reproductive Sciences (A.C., S.D.), Yale; University, School of Medicine, New Haven, Connecticut, USA.; Department of Experimental Pharmacology (R.M.), University of Naples "Federico; II", Naples, Italy 80131
* To whom correspondence should be addressed. E-mail: sabrina.diano{at}yale.edu.
During food deprivation, plasma thyroxine (T4) and triiodothyronine (T3) levels are decreased. Under this metabolic condition, hypothalamic deiodinase type 2 (D2) activity and mRNA levels are elevated while TSH-releasing hormone (TRH) mRNA levels are suppressed. Systemic T4 administration does not reverse these hypothalamic changes. The mechanism(s) that underlies this paradoxical regulation of D2 during fasting is unknown. We hypothesize that leptin and/or glucocorticoids play a role in these mechanisms and their interactions may be an important regulator of the hypothalamic-pituitary-thyroid axis. Thus, we assessed the effect of these hormones on D2 activity levels of food deprived as well as fed animals using enzyme activity measurements. In food deprived animals, corticosterone replacement reversed the inhibitory effect of adrenalectomy (ADX) on D2 induction, while ADX and ADX plus corticosterone replacement did not significantly affect D2 activity levels in rats fed ad libitum. Leptin administration in fed animals did not change D2 activity while, in fasted rats, leptin decreased D2 activity by reducing corticosterone plasma levels. When leptin was administered to fasted animals that were either ADX or ADX plus corticosterone treated at a high dose, D2 activity did not increase. Our results show that during fasting diminishing leptin levels play a permissive role to enable glucocorticoid-induced up-regulation of D2. Thus, our observations suggest that appropriate induction of D2 activity during negative energy balance is dependent upon both leptin and glucocorticoid signaling.
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