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Cytokine. 2019 Dec;124:154569. doi: 10.1016/j.cyto.2018.10.010. Epub 2018 Oct 30.

Hepatic growth hormone - JAK2 - STAT5 signalling: Metabolic function, non-alcoholic fatty liver disease and hepatocellular carcinoma progression.

Author information

1
Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria.
2
Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria; Medical University of Vienna, Vienna, Austria.
3
Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
4
Department of Clinical Pathology, Medical University of Vienna, Vienna, Austria.
5
Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria; Department of Clinical Pathology, Medical University of Vienna, Vienna, Austria; Institute of Laboratory Animal Pathology, University of Veterinary Medicine Vienna, Vienna, Austria.
6
Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria.
7
Diagnostic & Research Center for Molecular BioMedicine, Institute of Pathology, Medical University of Graz, Austria; Department of Pathology, Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany; Department of Pathology, Medical University of Innsbruck, Innsbruck, Austria.
8
Key Laboratory of Human Disease Comparative Medicine, the Ministry of Health; Institute of Laboratory Animal Sciences (ILAS), Chinese Academy of Medical Science (CAMS) and Peking Union Medical College (PUMC), Beijing, PR China; Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center (CCHMC), Cincinnati, OH, USA.
9
Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria; Ludwig Boltzmann Institute for Cancer Research, Vienna, Austria; Medical University of Vienna, Vienna, Austria. Electronic address: richard.moriggl@vetmeduni.ac.at.

Abstract

The rising prevalence of obesity came along with an increase in associated metabolic disorders in Western countries. Non-alcoholic fatty liver disease (NAFLD) represents the hepatic manifestation of the metabolic syndrome and is linked to primary stages of liver cancer development. Growth hormone (GH) regulates various vital processes such as energy supply and cellular regeneration. In addition, GH regulates various aspects of liver physiology through activating the Janus kinase (JAK) 2- signal transducer and activator of transcription (STAT) 5 pathway. Consequently, disrupted GH - JAK2 - STAT5 signaling in the liver alters hepatic lipid metabolism and is associated with NAFLD development in humans and mouse models. Interestingly, while STAT5 as well as JAK2 deficiency correlates with hepatic lipid accumulation, recent studies suggest that these proteins have unique ambivalent functions in chronic liver disease progression and tumorigenesis. In this review, we focus on the consequences of altered GH - JAK2 - STAT5 signaling for hepatic lipid metabolism and liver cancer development with an emphasis on lessons learned from genetic knockout models.

KEYWORDS:

Hepatic lipid metabolism; Liver; Liver cancer; NAFLD

PMID:
30389231
DOI:
10.1016/j.cyto.2018.10.010
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