Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2003) 5 P169

BES2003 Poster Presentations Growth and Development (16 abstracts)

Expression and distribution of the prolactin-receptor in healthy, fibrotic and cirrhotic liver in rats and humans

S Kloehn , J Simon-Holtorf , J Bachmann & H Mönig

Department of Internal Medicine, University of Kiel, Germany.

In patients with cirrhosis, levels of prolactin are often increased, which can be related to the disturbed metabolism of estrogens. According to recent results, prolactin presumably has its role as a factor for regeneration and the induction of growth-associated genes (e.g.: c-myc, c-fos, c-jun). To learn about the function of PRL in the pathogenesis of cirrhosis we focused on the conduct of the prolactin-receptor (PRL-R) during reconstruction from healthy liver parenchyma to fibrotic and then cirrhotic liver in rats and humans.
We treated 30 rats with CCl4 and supplemented Phenobarbitone for enzyme induction. Two groups with 30 animals each, that were either treated with phenobarbitone only or received no treatment at all, served as controls. After 35, 50, and 70 days 20 animals of each group were killed and liver tissue was taken out for performance of PCR, histological and immunhistochemical studies. Samples of human livers were directly taken out of 36 explanted livers while transplantation procedures (local Ethical Committee approval has been obtained). The expression of PRL-R was measured by means of mRNA-extraction, RT-PCR and computer-assisted densitometric evaluation. Distribution of PRL-R was demonstrated immunhistochemically.
Results of human and rat livers were the same. The histological evaluation showed different degrees from fibrosis to complete cirrhosis. Refering to controls the expression of RPL-R was increased in cirrhotic livers, though the strongest augmentation was seen in fibrotic tissues. Immunhistochemically the PRL-R was demonstrated in normal liver parenchyma, in the epithelium of the biliary ducts and around the central veins. This distribution did not exist in fibrotic and cirrhotic tissue. In those samples an accumulation could be seen in the damaged hepatocytes.
Therefore, we assume that PRL takes in a metabolic function in healthy liver parenchyma and might play a role in the pathogenesis of liver cirrhosis during the reconstruction of tissue. Results that were gained in experimental studies on rats were transferable on human conditions.

Volume 5

22nd Joint Meeting of the British Endocrine Societies

British Endocrine Societies 

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