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Alvaro Souto Padron, Ruy Andrade Louzada Neto, Thiago Urgal Pantaleão, Maria Carolina de Souza dos Santos, Renata Lopes Araujo, Bruno Moulin de Andrade, Monique da Silva Leandro, João Pedro Saar Werneck de Castro, Andrea Claudia Freitas Ferreira, and Denise Pires de Carvalho

these unequivocal effects on energy metabolism, 3,5-T2 might also affect the hypothalamus–pituitary–thyroid axis. Horst et al . (1995) have shown that 3,5-T2 treatment reduced serum thyroid-stimulating hormone (TSH) and thyroxine (T 4 ) levels as well

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Anna de Lloyd, James Bursell, John W Gregory, D Aled Rees, and Marian Ludgate

The TSH receptor and its role in the thyroid The established biological function of the TSH receptor (TSHR) in the thyroid gland is to regulate synthesis and secretion of thyroid hormones from follicular thyroid cells; it also plays an important

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Min Lu and Reigh-Yi Lin

primarily from physical inactivity and a reduced resting metabolic rate by virtue of the accompanying dramatic elevations of thyroid-stimulating hormone (TSH) levels. Sub-clinical hypothyroidism, characterized by elevated TSH levels but normal thyroid

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P C Lisboa, E de Oliveira, A C Manhães, A P Santos-Silva, C R Pinheiro, V Younes-Rapozo, L C Faustino, T M Ortiga-Carvalho, and E G Moura

thyrotropin (TSH), featuring a primary thyroid hypofunction, as well as higher serum leptin in the suckling pups, at the end of nicotine exposure. Interestingly, these animals show a very quick recovery at weaning, because these parameters were normal. In

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Beate Karges, Gerd Krause, Janos Homoki, Klaus-Michael Debatin, Nicolas de Roux, and Wolfram Karges

Introduction The thyrotrophin receptor (TSH-R) belongs to the family of G protein-coupled receptors (GPCRs) containing seven transmembrane helices (TMH). Since 1994, activating germline mutations of the TSH-R have been identified as

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Takao Ando, Rauf Latif, and Terry F Davies

uncleaved holoreceptors on the cell surface than seen in thyroid cells ( Misrahi et al. 1994 , Rapoport et al. 1998 ). Deletion of the cleaved region in the TSHR ectodomain does not affect TSH binding to, nor activation of, the TSHR ( Chazenbalk et al

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Patricia Joseph-Bravo, Lorraine Jaimes-Hoy, Rosa-María Uribe, and Jean-Louis Charli

, although the purification and identification of thyroid-stimulating hormone (TSH) spanned several decades ( Magner 2014 ). Semi-purified TSH preparations from bovine pituitaries demonstrated a similar structure to other pituitary hormones. It is composed of

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Alessandro Marsili, Edith Sanchez, Praful Singru, John W Harney, Ann Marie Zavacki, Ronald M Lechan, and P R Larsen

Introduction The feedback regulation of TSH secretion by thyroid hormones is mediated by the binding of 3,3′,5′-triiodothyronine (T 3 ) to the TRβ2 receptor in the pituitary and hypothalamus ( Chiamolera & Wondisford 2009 ). The acute suppression of

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Emin Umit Bagriacik, Melek Yaman, Rauf Haznedar, Gulsan Sucak, and Tuncay Delibasi

Introduction The TSH receptor or the thyrotropin receptor (TSHR) is usually expressed by thyroid cells. It is a G protein-coupled receptor and signals through cAMP and inositol triphosphate (IP 3 ) pathways ( Kursawe & Paschke 2000 , Davies et al

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L Schaaf, J Trojan, T E Helton, K H Usadel, and J A Magner


The aims of the present study were to determine the influence of brief subclinical hypothyroidism on the isoforms of serum thyrotropin (TSH) and to examine the net charge of TSH in different metabolic states. Sera were obtained from euthyroid subjects (n=7) and from patients with subclinical hypothyroidism (n=8) before and 30 min after the intravenous administration of 200 μg thyrotropin-releasing hormone (TRH). The TSH from human pituitary extracts (IRP 68/38), basal and TRH-stimulated serum TSH was immunoconcentrated and further analysed by isoelectric focusing (IEF) and lentil lectin affinity chromatography. TSH immunoreactivity was determined in each specimen or fraction with an automated highly sensitive chemiluminometric TSH assay. We found that basal TSH in subclinical hypothyroidism, and TRH-released TSH in euthyroidism and in subclinical hypothyroidism is distributed in a similar neutral to acidic pattern, which significantly differs from the more alkaline to neutral isoform pattern of intrapituitary TSH (P<0·05). IEF analysis of pituitary standard TSH revealed 3 major peaks (pI values 7·5; 6·6; 5·8) whereas in most euthyroid or subclinically hypothyroid subjects 5 peaks were found. Lentil lectin affinity chromatography revealed that TRH-released TSH in euthyroid subjects has more core fucose residues than TSH from patients with subclinical hypothyroidism (64·6 ±6·7 vs 12·5 ±2·7%, P<0·0001).

Thus pituitary standard TSH seems to be less mature material than circulating TSH. Perhaps no alteration in the IEF pattern of TSH was detected during early hypothyroidism because sialylation of TSH was increasing as sulfatation was decreasing. Nevertheless, a change in the core fucose content of TSH was detectable by lentil analysis.

Journal of Endocrinology (1995) 144, 561–567