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Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100DD, Amsterdam, The Netherlands
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Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100DD, Amsterdam, The Netherlands
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Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100DD, Amsterdam, The Netherlands
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Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100DD, Amsterdam, The Netherlands
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Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100DD, Amsterdam, The Netherlands
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Department of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100DD, Amsterdam, The Netherlands
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Introduction Tri-iodothyronine (T 3 ) affects cardiac function mainly by exerting a direct effect on cardiac cells through binding to thyroid hormone receptors (TR), thus regulating several functionally important proteins responsible
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induced by high-fat diet ingestion are attenuated ( Baur et al . 2006 , Feige et al . 2008 , Pfluger et al . 2008 ). However, at this point in time, our knowledge on SIRT1 protein expression regulation is limited. Similar to SIRT1, thyroid hormones
Department of Neuroendocrinology, Max-Planck-Institute for Experimental Endocrinology, Feodor-Lynen-Str. 7, 30625 Hannover, Germany
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Department of Neuroendocrinology, Max-Planck-Institute for Experimental Endocrinology, Feodor-Lynen-Str. 7, 30625 Hannover, Germany
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Department of Neuroendocrinology, Max-Planck-Institute for Experimental Endocrinology, Feodor-Lynen-Str. 7, 30625 Hannover, Germany
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Department of Neuroendocrinology, Max-Planck-Institute for Experimental Endocrinology, Feodor-Lynen-Str. 7, 30625 Hannover, Germany
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Department of Neuroendocrinology, Max-Planck-Institute for Experimental Endocrinology, Feodor-Lynen-Str. 7, 30625 Hannover, Germany
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Department of Neuroendocrinology, Max-Planck-Institute for Experimental Endocrinology, Feodor-Lynen-Str. 7, 30625 Hannover, Germany
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Department of Neuroendocrinology, Max-Planck-Institute for Experimental Endocrinology, Feodor-Lynen-Str. 7, 30625 Hannover, Germany
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Introduction Thyroid hormones (TH) are essential for development, growth, metabolism, and reproduction ( Porterfield & Hendrich 1993 , Oppenheimer & Schwartz 1997 , Anderson et al. 2003 , Choksi et al. 2003 , Bernal 2005
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collected fecal samples. Researchers have recently measured thyroid hormones (THs) in fecal samples in a validation study across several mammalian species ( Wasser et al. 2010 ), in response to reduced food availability ( Ingbar & Galton 1975 , Abdullah
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in EO animals. Therefore, we aimed to investigate the long-term effects of postnatal EO on thyroid hormone (TH) metabolism by evaluating the D1 and D2 activities in different tissues. By investigating these long-term effects, we can enhance our
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Laboratory of Endocrine Physiology, Laboratory of Neurophysiology, Carlos Chagas Filho Biophysic Institute, Biology Institute, State University of Rio de Janeiro, Rio de Janeiro 20551‐030, Brazil
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adrenal function and serum glucocorticoid levels with higher levels of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) in adult offspring whose mothers were nicotine-exposed (Pinheiro et al . 2011). Thyroid hormones (THs), T 4
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addressed the implication of fetal malnutrition for hypothalamic–pituitary–thyroid function later in life and results have been contradictory as presented in the following. Thyroid hormones (THs) are required for normal function and development of nearly all
Max Planck Institute for Experimental Endocrinology, Department of Cell and Molecular Biology, Fritz-Lipmann-Institut, Institute of Biomedicine, Institute for Biochemistry, University of East Anglia, Feodor-Lynen-Str. 7, D-30625 Hannover, Germany
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Max Planck Institute for Experimental Endocrinology, Department of Cell and Molecular Biology, Fritz-Lipmann-Institut, Institute of Biomedicine, Institute for Biochemistry, University of East Anglia, Feodor-Lynen-Str. 7, D-30625 Hannover, Germany
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also in the pituitary of the athyroid Pax8 −/− mouse. These mice lack the thyroid hormone (TH) producing follicular cells of the thyroid gland and are thus completely athyroid in postnatal life ( Mansouri et al . 1998 ). These mutants can therefore be
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Thyroid hormones (THs) regulate growth, development, differentiation and metabolic processes by interacting and activating thyroid hormone receptors (TRs). Although much progress has been made in our understanding of the transcriptional regulation of many TR target genes, little is known of the regulation of plasma protein gene expression by TRs. To investigate the role of TRs in plasma protein expression we used human hepatocellular carcinoma cell lines and carried out cDNA microarray analysis. Our results indicate that several plasma proteins including transferrin, prothrombin, angiotensinogen, haptoglobin, alpha-2-HS-glycoprotein alpha and beta chain, complement, lipoproteins and fibrinogen are up-regulated by THs. Furthermore, clusterin, alpha-2-macroglobulin precursor, prothymosin alpha and alpha-fetoprotein were found to be down-regulated by THs.Transferrin, an iron-binding protein expressed in all mammals, and mainly synthesized in the liver, was investigated further. Immunoblot and Northern blot analyses revealed that exposure of HepG2-TRalpha1 sub-lines and HepG2-Neo cells to tri-iodothyronine (T(3)) induced time- and dose-dependent increases in the abundance of transferrin mRNA and protein, with the extent of these effects correlating with the level of expression of TRalpha1. Nuclear run-on experiments indicate that this induction is functioning at the transcriptional level. Moreover, cyclohexamide treatment did not eliminate the induction of transferrin by TH. Thus, our results suggest that the induction of transferrin by TH is direct and may in fact be mediated by an as yet unidentified response element in the promoter region.
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persistently decreased serum thyroid hormones via decreased pituitary thyroid-stimulating hormone (TSH) subunit mRNA expression ( Wiersinga 2005 ). The observed modest increase in hypothalamic D2 activity during fasting ( Diano et al. 1998 ) is in
