Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Shoda, J. et al.

Primary dual defect of cholesterol and bile acid metabolism in liver of patients with intrahepatic calculi.

BACKGROUND/AIMS: Intrahepatic calculi, which are characterized by cholesterol-rich pigment stones, are highly prevalent in East Asia. Their pathogenesis remains unknown. To elucidate the etiological factors underlying the formation of cholesterol-supersaturated bile, which leads to the formation of cholesterol-rich pigment stones cholesterol and bile acid de novo syntheses in the liver were studied. METHODS: Liver specimens were assayed for the catalytic activities and steady-state messenger RNA levels of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and cholesterol 7 alpha-hydroxylase. RESULTS: The activity of HMG-CoA reductase, consistent with the messenger RNA level, was significantly higher in 13 patients with intrahepatic grown pigment stones (11.2 +/- 1.3 pmol.min-1.mg protein-1 [mean +/- SEM; P < 0.0001] for affected hepatic lobes and 13.4 +/- 1.7 [P < 0.0001] for unaffected ones [P < 0.0001]) than in 19 control subjects (6.4 +/- 0.4) and in 29 patients with gallbladder cholesterol stones (2.1 +/- 0.1). On the other hand, the activity of 7 alpha-hydroxylase, consistent with the messenger RNA level, was significantly lower in patients with intrahepatic brown pigment stones (2.8 +/- 0.5 pmol.min-1.mg protein-1 [P < 0.0001] for affected lobes and 2.6 +/- 0.5 [P < 0.0001] for unaffected ones) than in control subjects (6.0 +/- 0.6) and in patients with cholesterol stones (5.1 +/- 0.5). CONCLUSIONS: In intrahepatic calculi, the formation of supersaturated bile and cholesterol-rich pigment stones may be attributed to the primary dual defect of up-regulated cholesterogenesis and down-regulated bile acid synthesis in the liver.[1]

References

Primary dual defect of cholesterol and bile acid metabolism in liver of patients with intrahepatic calculi. Shoda, J., He, B.F., Tanaka, N., Matsuzaki, Y., Yamamori, S., Osuga, T. Gastroenterology (1995) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.