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Possible roles of insulin-like growth factor in regulation of physiological and pathophysiological liver growth.

Artikel i vetenskaplig tidskrift
Författare Stanko Skrtic
Kristina Wallenius
Klara Sjögren
Olle Isaksson
Claes Ohlsson
John-Olov Jansson
Publicerad i Hormone research
Volym 55 Suppl 1
Sidor 1-6
ISSN 0301-0163
Publiceringsår 2001
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för internmedicin
Institutionen för invärtesmedicin
Institutionen för invärtesmedicin, Avdelningen för klinisk farmakologi
Sidor 1-6
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Cell Division, physiology, Culture Media, Conditioned, pharmacology, DNA, biosynthesis, Hepatocyte Growth Factor, biosynthesis, genetics, Hepatocytes, cytology, pathology, Liver, cytology, growth & development, metabolism, pathology, Liver Diseases, physiopathology, Mice, Mice, Knockout, genetics, Mitogens, pharmacology, Somatomedins, deficiency, physiology
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

BACKGROUND/AIMS: Almost all circulating insulin-like growth factor-1 (IGF-1) is produced and secreted from the liver. However, the possible role of IGF-1 in local regulation of liver functions including liver growth is unclear. In the present study, we investigated the role of IGF-1 on liver growth in vivo and in hepatic stellate cell function in vitro. RESULTS: Liver-specific knock-out of the IGF-1 gene by use of the cre-loxP system caused enhanced liver growth, possibly reflecting increased growth hormone (GH) secretion due to decreased negative feedback by IGF-1. Studies on cultured rat hepatic stellate cells (HSC) showed that IGF-1 and hepatocyte-conditioned medium (PCcM) time- and dose-dependently increased hepatocyte growth factor (HGF) mRNA and HGF immunoreactivity. IGF-1 and PCcM also enhanced DNA synthesis in the HSC cultures. The PCcM did not contain bioactive IGF-1 and was also able to stimulate proliferation when prepared under serum- and hormone-free conditions. CONCLUSION: In vivo results show that IGF-1 is not essential for normal growth of the intact liver. The in vitro results indicate that both IGF-1 and IGF- 1-independent factor(s) from hepatocytes can stimulate HGF production by HSC. It remains to be investigated whether these effects are of importance for liver regeneration or pathological conditions.

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