Biological efficacy of partial hepatectomy and hepatopoietin in long-term selenium-deficient mice.
After partial hepatectomy the normal low proliferation rate of hepatocytes increases dramatically. This is based on a feed-back system whose central link is a liver cell proliferation hormone, the so-called hepatopoietin. This glycoprotein is organ-specific but not species-specific, i.e. an extract from rats is also active in mice. In order to examine the influence of selenium on liver cell proliferation, male albino NMRI mice were fed a selenium-deficient diet containing less than 10 ppb Se for at least 2 months (Se-). In the plasma protein profile and in the basic DNA synthesis rate of Se(-)-animals, no significant changes were observed compared to controls. However, liver cell proliferation induced by hepatopoietin or by partial hepatectomy was increased about 3-fold in Se-deficient mice. We assume a compensated metabolic Se-deficiency state in mice under these nutritional conditions, which leads to expression of enhanced metabolic capacity when induced by stress.
D000818:Animals; D001798:Blood Proteins / Q000378:metabolism / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects; D004247:DNA / Q000378:metabolism; D005260:Female; D006498:Hepatectomy; D017228:Hepatocyte Growth Factor; D008099:Liver / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051379:Mice; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium / Q000172:deficiency* / Q000378:metabolism
D001798:Blood Proteins; D017228:Hepatocyte Growth Factor; D004247:DNA; D012643:Selenium