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A more recent version of this article appeared on July 1, 2003

Papers In Press, published online ahead of print April 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300030-JLR200
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Submitted on January 21, 2003
Revised on April 4, 2003
Accepted on April 15, 2003

Stimulation of cholesterol synthesis and hepatic lipogenesis in patients with severe malabsorption

Ana Cachefo, Philippe Boucher, Eric Dusserre, Paul Bouletreau, Michel Beylot, and Cécile Chambrier

INSERM U 499, Faculté Laennec, Lyon 69008

Corresponding Author: beylot{at}laennec.univ-lyon1.fr

Patients with severe malabsorption have abnormal lipid metabolism with low plasma cholesterol and frequently high triglycerides levels. The mechanisms behind these abnormalities and the respective roles of malabsorption itself and of the parenteral nutrition given to these patients are unclear. We measured endogenous lipids synthesis (cholesterol synthesis and hepatic lipogenesis) and the expression (mRNA concentrations in circulating mononuclear cells) of regulatory genes of cholesterol metabolism in 10 control subjects and 22 patients with severe malabsorption receiving (n=18) or weaned of parenteral nutrition (n=4). Patients had low plasma cholesterol (p<0.01) and raised triglycerides (p<0.05) levels. Both fractional and absolute cholesterol synthesis (p<0.001) and hepatic lipogenesis (p<0.01) were increased. These abnormalities are independent of parenteral nutrition since they were present in patients receiving or weaned of parenteral nutrition. No relation between hepatic lipogenesis and plasma TG levels was found suggesting that other metabolic abnormalities participated to hypertriglyceridemia. HMG-CoA reductase and LDL-receptor mRNA levels were decreased (p<0.05) in patients on long term parenteral nutrition. HMG-CoA reductase mRNA were normal in weaned patients. Conclusions: Severe malabsorption induces large increases of cholesterol synthesis and hepatic lipogenesis, independently of the presence of parenteral nutrition. These abnormalities are probably due to the malabsorption of bile acids.


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