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Key Laboratory of Aquatic Biodiversity and Conservation of Chinese Academy of Sciences, University of Chinese Academy of Sciences, Institute of Hydrobiology, Chinese Academy of Sciences, 7 Donghu South Road, Wuhan, Hubei 430072, People's Republic of China
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Key Laboratory of Aquatic Biodiversity and Conservation of Chinese Academy of Sciences, University of Chinese Academy of Sciences, Institute of Hydrobiology, Chinese Academy of Sciences, 7 Donghu South Road, Wuhan, Hubei 430072, People's Republic of China
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Key Laboratory of Aquatic Biodiversity and Conservation of Chinese Academy of Sciences, University of Chinese Academy of Sciences, Institute of Hydrobiology, Chinese Academy of Sciences, 7 Donghu South Road, Wuhan, Hubei 430072, People's Republic of China
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, the transcriptional levels of other neuropeptide signaling molecules, including Ssts and Sst receptors, Ghrh and Ghrh receptors, Npy receptors, thyrotropin-releasing hormone (Trh) and Trh receptors, corticotrophin-releasing hormone (Crh) and Crh
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three hypothalamic regulatory peptide neurohormones: thyrotrophin-releasing factor (now thyrotrophin-releasing hormone, TRH), LH- and follicle-stimulating hormone (FSH)-releasing factor (now gonadotrophin-releasing hormone, GnRH) and somatostatin
Local impact of thyroid hormone inactivation
Deiodinases: the balance of thyroid hormone
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may promote a local central hyperthyroidism by oppositely regulating D2 and D3, which in turn leads to a negative feedback control on TRH synthesis in hypophysiotropic neurons. In this scenario, D3 may be involved in the low TSH seen in inflammation
Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Nagoya, Japan
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Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Nagoya, Japan
Division of Seasonal Biology, National Institute for Basic Biology, Okazaki, Japan
Avian Bioscience Research Center, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan
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hypothalamic–pituitary–thyroid (HPT) axis. Thyrotropin-releasing hormone (TRH) secreted from the hypothalamus induces the pars distalis of the anterior pituitary gland to release thyroid-stimulating hormone (TSH), which in turn stimulates the thyroid gland to
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specific receptors in the arcuate nucleus of the hypothalamus, induce neuroendocrine changes resulting in increased release of TRH from the hypothalamus, TSH from the pituitary gland, and thereby TH from the thyroid glands ( Costa da Veiga et al . 2004
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. References Arimura A Schally AV 1976 Increase in basal and thyrotropin-releasing hormone (TRH)-stimulated secretion of thyrotropin (TSH) by passive immunization with antiserum to somatostatin in rats . Endocrinology 98 1069 – 1072 . ( doi:10
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lactation . Reproductive Sciences 19 493 – 504 . ( doi:10.1177/1933719111424439 ) Sarr O Yang K Regnault TRH 2012 In utero programming of later adiposity: the role of fetal growth restriction . Journal of Pregnancy 2012 134758 . ( doi:10
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, Ladram A & Aratan de Leon S 1999 Triiodothyronine down regulates thyrotropin-releasing hormone (TRH) synthesis and decreases pTRH-(160–169) and insulin release from fetal rat islets in culture. Endocrinology 140 4113 –4119
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Regnault TRH Wilkening RB Meschia G Battaglia FC 2004 Placental uptake and transport of ACP, a neutral nonmetabolizable amino acid, in an ovine model of fetal growth restriction . American Journal of Physiology: Endocrinology and
Department of Physiology, Department of Biological and Medical Sciences, Development and Neuroscience, University of Cambridge, Physiology Building, Downing Street, Cambridge CB2 3EG, UK
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hormones in the fetus, placenta, and mother. TRH, thyrotropin-releasing hormone; TSH, thyroid-stimulating hormone; T 4 , thyroxine; T 3 , triiodothyronine; rT 3 , reverse T 3 ; T 2 , diiodothyronine; S, sulfated; D1, D2, and D3, deiodinases; OATP, organic
