Universität zu Köln

Mueller, Kristina M., Themanns, Madeleine, Friedbichler, Katrin, Kornfeld, Jan-Wilhelm ORCID: 0000-0002-6802-4442, Esterbauer, Harald, Tuckermann, Jan P. and Moriggl, Richard ORCID: 0000-0003-0918-9463 (2012). Hepatic growth hormone and glucocorticoid receptor signaling in body growth, steatosis and metabolic liver cancer development. Mol. Cell. Endocrinol., 361 (1-2). S. 1 - 12. CLARE: ELSEVIER IRELAND LTD. ISSN 0303-7207

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Abstract

Growth hormone (GH) and glucocorticoids (GCs) are involved in the control of processes that are essential for the maintenance of vital body functions including energy supply and growth control. GH and GCs have been well characterized to regulate systemic energy homeostasis, particular during certain conditions of physical stress. However, dysfunctional signaling in both pathways is linked to various metabolic disorders associated with aberrant carbohydrate and lipid metabolism. In liver, GH-dependent activation of the transcription factor signal transducer and activator of transcription (STAT) 5 controls a variety of physiologic functions within hepatocytes. Similarly, GCs, through activation of the glucocorticoid receptor (GR), influence many important liver functions such as gluconeogenesis. Studies in hepatic Stat5 or GR knockout mice have revealed that they similarly control liver function on their target gene level and indeed, the GR functions often as a cofactor of STAT5 for CH-induced genes. Gene sets, which require physical STAT5-GR interaction, include those controlling body growth and maturation. More recently, it has become evident that impairment of GH-STAT5 signaling in different experimental models correlates with metabolic liver disease, ranging from hepatic steatosis to hepatocellular carcinoma (HCC). While GH-activated STAT5 has a protective role in chronic liver disease, experimental disruption of GC-GR signaling rather seems to ameliorate metabolic disorders under metabolic challenge. In this review, we focus on the current knowledge about hepatic CH-STAT5 and GC-GR signaling in body growth, metabolism, and protection from fatty liver disease and HCC development. (c) 2012 Elsevier Ireland Ltd. All rights reserved.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Mueller, Kristina M. UNSPECIFIED UNSPECIFIED UNSPECIFIED Themanns, Madeleine UNSPECIFIED UNSPECIFIED UNSPECIFIED Friedbichler, Katrin UNSPECIFIED UNSPECIFIED UNSPECIFIED Kornfeld, Jan-Wilhelm UNSPECIFIED orcid.org/0000-0002-6802-4442 UNSPECIFIED Esterbauer, Harald UNSPECIFIED UNSPECIFIED UNSPECIFIED Tuckermann, Jan P. UNSPECIFIED UNSPECIFIED UNSPECIFIED Moriggl, Richard UNSPECIFIED orcid.org/0000-0003-0918-9463 UNSPECIFIED
URN:	urn:nbn:de:hbz:38-482800
DOI:	10.1016/j.mce.2012.03.026
Journal or Publication Title:	Mol. Cell. Endocrinol.
Volume:	361
Number:	1-2
Page Range:	S. 1 - 12
Date:	2012
Publisher:	ELSEVIER IRELAND LTD
Place of Publication:	CLARE
ISSN:	0303-7207
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language NONALCOHOLIC FATTY LIVER; CORTICOSTEROID-BINDING GLOBULIN; PITUITARY-ADRENAL AXIS; ACID-LABILE SUBUNIT; TRANSGENIC MICE; HEPATOCELLULAR-CARCINOMA; INSULIN-RESISTANCE; TRANSCRIPTION FACTORS; ADIPOSE-TISSUE; DNA-BINDING Multiple languages Cell Biology; Endocrinology & Metabolism Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/48280