regulated by thyrotrophin (TSH) mainly by the modulation of thyroid-specific genes, such as NIS, TG and TPO ( Dunn & Dunn 2001 ). The existence of a basal tonic level of endogenous NO generation with a possible autocrine or paracrine role in the
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Laura Fozzatti, María L Vélez, Ariel M Lucero, Juan P Nicola, Iván D Mascanfroni, Daniela R Macció, Claudia G Pellizas, Germán A Roth, and Ana M Masini-Repiso
Elaine Cristina Lima de Souza, Álvaro Souto Padrón, William Miranda Oliveira Braga, Bruno Moulin de Andrade, Mário Vaisman, Luiz Eurico Nasciutti, Andrea Claudia Freitas Ferreira, and Denise Pires de Carvalho
physiology. The ability of the thyroid gland to accumulate radioiodine is also important for the diagnosis and treatment of thyroid disorders ( Mazaferri 2000 ). TSH is the major regulator of thyroid cell proliferation, differentiation, and function
Nadia Schoenmakers, Kyriaki S Alatzoglou, V Krishna Chatterjee, and Mehul T Dattani
Introduction Central congenital hypothyroidism (CCH) is a rare disorder in which inadequate thyroid hormone biosynthesis occurs due to defective stimulation of a normal thyroid gland by thyroid stimulating hormone (TSH). The underlying molecular
Eleonore Fröhlich, Anja Witke, Barbara Czarnocka, and Richard Wahl
(TSH)-induced uptake of iodide and the release of organified iodine in normal human thyrocytes ( Namba et al. 1993 ). High concentrations of retinol also exert dedifferentiating effects on normal thyrocytes ( Fröhlich et al. 2001 ). These effects
K J Oliveira, G S M Paula, R H Costa-e-Sousa, L L Souza, D C Moraes, F H Curty, and C C Pazos-Moura
intracerebroventricular administration of NPY to normally fed rats resulted in reduction of circulating levels of thyroid hormones with inappropriately normal or low thyrotropin (TSH), and suppression of proTRH mRNA in the hypothalamic paraventricular nucleus (PVN
Andrea C F Ferreira, Lívia P Lima, Renata L Araújo, Glaucia Müller, Renata P Rocha, Doris Rosenthal, and Denise P Carvalho
underlying the control of NIS expression, and the regulation of its activity in the plasma membrane. The ability of the thyroid gland to concentrate iodine has been known for several decades and many reports have demonstrated that thyrotrophin (TSH
J Fahrenkrug, B Georg, J Hannibal, and H L Jørgensen
the cytoplasm, CRY and PER proteins translocate into the nucleus and form inhibitory complexes feeding negatively back on their own transcription. A daily rhythmicity of circulating thyroid-stimulating hormone (TSH) peaking at daytime in rats is well
D C Ferguson, Z Caffall, and M Hoenig
et al. 1991 , Silva 1995 ). However, studies of thyroid function in obese people have produced inconsistent results. Obesity has resulted in either no changes in thyroid-stimulating hormone (TSH) or TH concentrations in the hands of some
Thierry Métayé, Pierre Levillain, Jean-Louis Kraimps, and Rémy Perdrisot
) the β-adrenergic receptor kinases (GRK2 and GRK3), and 3) the GRK4, GRK5, and GRK6 subfamily ( Ribas et al . 2007 ). The thyrotropin (TSH) receptor belongs to the GPCR family and is a major determinant of thyroid function ( Vassart & Dumont 1992
Sisi Luan, Wenkai Bi, Shulong Shi, Li Peng, Zhanbin Li, Jie Jiang, Ling Gao, Yifeng Du, Xu Hou, Zhao He, and Jiajun Zhao
Introduction Thyroid hormones are produced and released by the thyroid gland, which regulate the metabolism of the body. The endocrine function of the thyroid gland is mediated by TSH, a glycoprotein hormone produced by the anterior pituitary
