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Submitted on July 28, 2005
Accepted on September 23, 2005
Tupper Research Institute and Department of Medicine, Division of Endocrinology, Diabetes, Metabolism and Molecular Medicine, New England Medical Center, 750 Washington St, Boston, MA, 02111; Department of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary; Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Boston, MA 02115; Division of Endocrinology, Universiade Federal de Sao Paulo, Sao Paulo, Brazil; Department of Community Health, Tufts University School of Medicine, Boston. MA 02111; Division of Endocrinology, University of Massachusetts Medical School, Worcester, MA 01655; Department of Neuroscience, Tufts University School of Medicine, Boston, MA 02111
* To whom correspondence should be addressed. E-mail: rlechan{at}tufts-nemc.org.
The reduction in circulating levels of leptin, insulin and glucose with fasting serve as important homeostasis signals to NPY/AGRP- and 
-MSH/ CART-synthesizing neurons of the hypothalamic arcuate nucleus. As the central administration of leptin is capable of restoring the inhibitory effects of fasting on TRH mRNA in hypophysiotropic neurons primarily through effects on the arcuate nucleus, we determined whether the continuous administration of 30 mU/d insulin or 648 µg/d glucose into the CSF by osmotic minipump might also have similar effects on the hypothalamic-pituitary-thyroid (HPT) axis. As anticipated, the icv infusion of leptin reduced fasting-induced elevations in NPY and AGRP mRNA and increased POMC and CART mRNA in the arcuate nucleus. In addition, leptin prevented fasting-induced reduction in proTRH mRNA levels in the PVN and in circulating thyroid hormone levels. In contrast, whereas insulin increased POMC mRNA and both insulin and glucose reduced NPY mRNA in arcuate nucleus neurons, neither prevented the fasting-induced suppression in hypophysiotropic TRH mRNA nor circulating thyroid hormone levels. We conclude that insulin and glucose only partially replicate the central effects of leptin and may not be essential components of the HPT regulatory system during fasting.
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