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intake and expenditure ( Ramos-Lobo & Donato 2017 ). Thus, genetic mutations that cause the absence of leptin or the leptin receptor (LepR) produce metabolic changes that resemble those observed during intense negative energy balance, including hunger and
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exerted by estradiol ( Kansra et al. 2005 ), several hypothalamic factors are also involved, including thyrotropin-releasing hormone (TRH), serotonin, oxytocin and VIP. While sex differences have been described in the maturation of these hypothalamic
Istituto di Endocrinologia e Oncologia Sperimentale G Salvatore, CNR, Naples, Italy
Dipartimento di Biologia e Patologia Cellulare e Molecolare L Califano, Naples, Italy
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Istituto di Endocrinologia e Oncologia Sperimentale G Salvatore, CNR, Naples, Italy
Dipartimento di Biologia e Patologia Cellulare e Molecolare L Califano, Naples, Italy
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Istituto di Endocrinologia e Oncologia Sperimentale G Salvatore, CNR, Naples, Italy
Dipartimento di Biologia e Patologia Cellulare e Molecolare L Califano, Naples, Italy
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Istituto di Endocrinologia e Oncologia Sperimentale G Salvatore, CNR, Naples, Italy
Dipartimento di Biologia e Patologia Cellulare e Molecolare L Califano, Naples, Italy
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Istituto di Endocrinologia e Oncologia Sperimentale G Salvatore, CNR, Naples, Italy
Dipartimento di Biologia e Patologia Cellulare e Molecolare L Califano, Naples, Italy
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Istituto di Endocrinologia e Oncologia Sperimentale G Salvatore, CNR, Naples, Italy
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Istituto di Endocrinologia e Oncologia Sperimentale G Salvatore, CNR, Naples, Italy
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Introduction P2-purinergic agonists have important biological functions on several tissues, due to the wide distribution of their receptors and their ubiquitous nature, since they derive from the cytosol of damaged cells or
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biochemical abnormalities in myxedematous patients (Pitt-Rivers 1955, 1956, Trotter 1955 , 1956 ). Later studies showed that TA 3 potently reduces TSH secretion and TRH-receptor expression in mouse thyrotropic pituitary tumor cells ( Gershengorn et al
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Metabolism and Diabetes and Imaging Programs, Departments of Medical Biophysics, Pathology, Medicine, Lawson Health Research Institute, 268 Grosvenor Street, London, Ontario, Canada N6A 4V2
Metabolism and Diabetes and Imaging Programs, Departments of Medical Biophysics, Pathology, Medicine, Lawson Health Research Institute, 268 Grosvenor Street, London, Ontario, Canada N6A 4V2
Metabolism and Diabetes and Imaging Programs, Departments of Medical Biophysics, Pathology, Medicine, Lawson Health Research Institute, 268 Grosvenor Street, London, Ontario, Canada N6A 4V2
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secretory pathway are separated from constitutive and lysosomal proteins and are packaged into budding immature secretory granules. The process of sorting can occur at the TGN through interaction with a membrane-bound sorting receptor, or with membrane
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β sub-units of thyroid-stimulating hormone (TSH). These cells lack receptors for the hypothalamic thyrotropin-releasing hormone (TRH) ( Bockmann et al . 1997 ), and do not respond to conventional hypothalamic outputs. In mammals, the MT1 receptor co
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1869 , Laguesse 1893 ), e.g. somatostatin in δ-cells ( Luft et al . 1974 ) and thyrotrophin-releasing hormone (TRH) in β-cells ( Kawano et al . 1983 ). In some cases, the functional output of signalling via these peptides converges to a common effect
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been shown to induce TSH release in chickens, and somatostatin can diminish the CRH- and TRH-induced TSH response through the type 2 and type 5 somatostatin receptors ( Geris et al. 1996 , 2003 a , Geris et al. b , DeGroef et al. 2003
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Laboratório de Fisiologia Endócrina Doris Rosenthal, Laboratório de Biologia do Exercício, Instituto de Biofísica Carlos Chagas Filho and Instituto de Pesquisa Translacional em Saúde e Ambiente na Região Amazônica (INPeTAM), CCS-Bloco G- Cidade Universitria, Ilha do Fundo, Rio de Janeiro 21949-900, Brazil
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TSH regulation, strongly support the hypothesis that 3,5-T2 functions as an agonist of the β isoform of thyroid hormone receptor (TR) in vivo . Figure 4 Type 1 (D1) and type 2 (D2) iodothyronine deiodinase activities in control rats and rats treated
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-releasing hormone (GNRH), neuropeptide Y, and thyrotrophin-releasing hormone (TRH) stimulate the release of GH, effects that have been shown to be influenced by gonadal sex steroids and by the nutritional state of the animal ( Sherwood et al . 2000