Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (35)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Ledda-Columbano, G. M.
Right arrow Articles by Pani, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ledda-Columbano, G. M.
Right arrow Articles by Pani, P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1985 Oxford University Press

research-article

Enhancement of cholesterol synthesis and pentose phosphate pathway activity in proliferating hepatocyte nodules

Giovanna M. Ledda-Columbano 1, Amedeo Columbano, Sandra Dessì, Pierpaolo Coni, Caterina Chiodino and Paolo Pani

Istituto di Farmacologia e Patologia Biochimica, University of Cagliari Via Porcell 4, 09100 Cagliari, Italy

1To whom reprint requests should be sent

The endogenous synthesis of cholesterol in hepatocyte nodules, induced in male Wistar rats, by a single dose of the hepato-carcinogen diethylnitrosamine followed by a selection pro-cedure, was investigated and was compared with that in surrounding and control tissue. In addition, the activity of enzymes related to carbohydrate metabolism (glucose-6-phos-phate dehydrogenase, 6-phosphogluconate dehydrogenase, glucose-6-phosphatase and pyruvate kinase), was measured. Hepatocyte nodules showed a striking increase in their capacity for synthesizing cholesterol, in comparison to surrounding and control tissues, and an enhancement in the activity of the pentose phosphate pathway, as indicated by increased activity of glucose-6-phosphate dehydrogenase and of 6-phos-phogluconate dehydrogenase, and a concomitant decrease of glucose-6-phosphatase. The stimulation of cholesterol synthesis and of the pentose phosphate pathway was associated with increased incorporation of labelled thymidine into DNA. These data indicate that, among other metabolic disturbances, enhancement of cholesterol synthesis and of the pentose phosphate pathway, is accompanied by an increased proliferative capacity of hepatocyte nodules.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol. Endocrinol.Home page
E. Rico-Bautista, C. J. Greenhalgh, P. Tollet-Egnell, D. J. Hilton, W. S. Alexander, G. Norstedt, and A. Flores-Morales
Suppressor of Cytokine Signaling-2 Deficiency Induces Molecular and Metabolic Changes that Partially Overlap with Growth Hormone-Dependent Effects
Mol. Endocrinol., March 1, 2005; 19(3): 781 - 793.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol PatholHome page
M. W. Roomi, A. Columbano, G. M. Ledda-Columbano, and D. S. R. Sarma
Induction of the Placental Form of Glutathione S-Transferase by Lead Nitrate Administration in Rat Liver
Toxicol Pathol, February 1, 1987; 15(2): 202 - 205.
[Abstract] [PDF]

Home page
 Toxicol PatholHome page
A. Columbano, S. Dessi, G. M. Ledda-Columbano, C. Chiodino, P. Coni, P. Pani, and K. N. Rao
HMP-Shunt and Cholesterol Metabolism in Experimental Models Involving Normal and Preneoplastic Liver Growth
Toxicol Pathol, January 1, 1987; 15(1): 43 - 50.
[Abstract] [PDF]

Home page
 Toxicol PatholHome page
A. G. Schwartz, L. Pashko, and J. M. Whitcomb
Inhibition of Tumor Development by Dehydroepiandrosterone and Related Steroids
Toxicol Pathol, April 1, 1986; 14(3): 357 - 362.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.