NPY and MC4R signaling regulate thyroid hormone levels during fasting through both central and peripheral pathways
作者： Kristen R. Vella , Preeti Ramadoss , Francis S. Lam , Jamie C. Harris , Felix D. Ye
DOI: 10.1016/J.CMET.2011.10.009
关键词: Hypothalamus 、 Endocrinology 、 Melanocortin 、 Neuropeptide Y receptor 、 Hormone 、 Arcuate nucleus 、 Leptin 、 Internal medicine 、 Thyrotropin-releasing hormone 、 Melanocortin 4 receptor 、 Biology
摘要: Fasting-induced suppression of the hypothalamic-pituitary-thyroid (HPT) axis is an adaptive response to decrease energy expenditure during food deprivation. Previous studies demonstrate that leptin communicates nutritional status HPT through thyrotropin-releasing hormone (TRH) in paraventricular nucleus (PVN) hypothalamus. Leptin targets TRH neurons either directly or indirectly via arcuate pro-opiomelanocortin (POMC) and agouti-related peptide/neuropeptide Y (AgRP/NPY) neurons. To evaluate role these pathways vivo, we developed double knockout mice lack both melanocortin 4 receptor (MC4R) NPY. We show NPY required for fasting-induced Trh expression PVN. However, MC4R are activation hepatic metabolize T(4) fasting response. Thus, signaling play a key communication signals reduce thyroid levels centrally peripheral circuit.
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