Leptin Prevents Fasting-Induced Suppression of Prothyrotropin-Releasing Hormone Messenger Ribonucleic Acid in Neurons of the Hypothalamic Paraventricular Nucleus*

• DOI: 10.1210/endo.138.6.5209
• Publication Date: 2014-01-08T16:09:05Z
• Authors: Gábor Légrádi; Charles H. Emerson; Rexford S. Ahima; Jeffrey S. Flier; Ronald M. Lechan
• Keywords: Hypothalamic–pituitary–thyroid axis

Prolonged fasting is associated with a number of changes in the thyroid axis manifested by low serum T3 and T4 levels and, paradoxically, or normal TSH. This response is, at least partly, caused suppression proTRH gene expression neurons hypothalamic paraventricular nucleus (PVN) reduced TRH release. Because fall hormone can be blunted mice systemic administration leptin, we raised possibility that leptin may have an important role neuroendocrine regulation axis, through effects on hypophysiotropic producing proTRH. Adult male, Sprague-Dawley rats were either fed normally, fasted for 3 days, administered dose 0.5 μg/gm BW ip every 6 h. Fasted animals showed significant reduction plasma total free compared controls, restored toward leptin. Percent T4, but not percent T3, increased during fasting, further suggesting transthyretin did return to after administration. By semiquantitative analysis situ hybridization autoradiograms, messenger RNA medial parvocellular PVN was markedly suppressed [fed vs. fast fast/leptin (density units × 108): 8.5 ± 0.4, 3.2 0.2, 8.1 0.8]. In contrast, adjacent lateral hypothalamus do function remained unchanged any experimental manipulations. These findings indicate has selective, central action modulate hypothalamic-pituitary-thyroid regulating does peripheral thyroid-binding proteins. We propose circulating resets set point feedback inhibition hormones biosynthesis proTRH, thereby allowing adaptation starvation.