ARH orexigenic:anorexigenic peptide balance; iii) in the setting of the increased fetal cortisol levels, we have previously described ( Nijland et al . 2010 ) that IUGR increases fetal ARH glucocorticoid receptor (GR) expression; and iv) as STAT3
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Cun Li, Thomas J McDonald, Guoyao Wu, Mark J Nijland, and Peter W Nathanielsz
Asghar Ali, Callie M Swanepoel, Quinton A Winger, Paul J Rozance, and Russell V Anthony
). CSH has high affinity for prolactin (PRL) receptors as well as growth hormone (GH) receptors ( Handwerger & Freemark 2000 ), although a distinct CSH receptor may exist in fetal liver ( Freemark et al. 1987 , Hill et al. 1988 , Pratt et al. 1995
Marco Colella, Valeria Nittoli, Alfonsina Porciello, Immacolata Porreca, Carla Reale, Filomena Russo, Nicola Antonino Russo, Luca Roberto, Francesco Albano, Mario De Felice, Massimo Mallardo, and Concetta Ambrosino
tissue/cell-specific levels of T 3 and, finally, on TH receptors (THRs). Local T 3 levels depend on an ensemble of tissue/cell-specific factors, such as deiodinases and TH transporters, which is relatively independent of serum TH levels ( Colella et al
I M McGonnell and R C Fowkes
2005 ). In fish, as in other non-mammalian vertebrates, corticotrophin-releasing factor (CRF) stimulates not only corticotrophin release from the pituitary but also thyrotrophin release ( Seasholtz et al. 2002 ). Thyrotrophin-releasing hormone (TRH
Jens Mittag, Wiebke Oehr, Heike Heuer, Tuula Hämäläinen, Bent Brachvogel, Ernst Pöschl, and Karl Bauer
indicated that A5 not only enhances gonadotropin secretion following stimulation by gonadotrophin-releasing hormone (GnRH; Kawaminami et al . 2002 ), but also stimulates basal PRL secretion while counteracting thyrotrophin-releasing hormone (TRH) induced
Dominik Simon Botermann, Nadine Brandes, Anke Frommhold, Ina Heß, Alexander Wolff, Arne Zibat, Heidi Hahn, Rolf Buslei, and Anja Uhmann
binding of Hh ligands (e.g. mammalian Sonic, Indian or Desert Hh) to the receptor protein Patched1 (Ptch). This releases the inhibition of Smoothened (Smo), which results in translocation of Smo into the primary cilium and nuclear translocation of
E Mezosi, J Szabo, E V Nagy, A Borbely, E Varga, G Paragh, and Z Varga
Introduction Most effects of thyroid hormone are mediated by a direct modulation of gene activity via interaction of the thyroid hormone–nuclear receptor complex with specific DNA sequences ( Ojamaa et al. 1996 ). Several results
E Oliveira, E G Moura, A P Santos-Silva, A T S Fagundes, A S Rios, Y Abreu-Villaça, J F Nogueira Neto, M C F Passos, and P C Lisboa
out by our group concerning other programing models ( Passos et al . 2004 , Bonomo et al . 2007 ), in which BW changes were not accompanied by food intake alterations. Leptin and leptin receptors are both found in skeletal muscle ( Wang et al
Christophe Breton
nutrients (glucose and free fatty acid). Leptin, together with insulin, acts on its respective receptor Ob-Rb and insulin receptor (InsR), both linked to the common phosphatidylinositol 3-kinase (PI3K) pathway, to reduce the expression and release of
Taeko Nishiwaki-Ohkawa and Takashi Yoshimura
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
