J. Lipid Res.
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A more recent version of this article appeared on January 1, 2003

Papers In Press, published online ahead of print October 16, 2002
J. Lipid Res., doi:10.1194/jlr.M200200-JLR200
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Submitted on May 20, 2002
Revised on October 4, 2002
Accepted on October 10, 2002

Mechanisms of liver steatosis in rats with systemic carnitinedeficiency due to treatment with trimethylhydraziniumpropionate

Markus Spaniol, Priska Kaufmann, Konstantin Beier, Jenny Wuthrich, Michael Torok, Hubert Scharnagl, Winifried Marz, and Stephen Krahenbuhl

University Hospital, Basel CH-4031

Corresponding Author: kraehenbuehl{at}uhbs.ch

Summary Background: Rats with systemic carnitine deficiency induced by treatment with trimethylhydraziniumpropionate (THP) develop liver steatosis. Aims: To investigate the mechanisms leading to steatosis in THP-induced carnitine deficiency. Methods: Rats were treated with THP (20 mg/100 g) for 3 or 6 weeks, and were studied after starvation for 24 hours. Results: Rats treated with THP had reduced in vivo palmitate metabolism and developed mixed liver steatosis at both time points. The hepatic carnitine pool was reduced in THP-treated rats by 65 to 75% at both time points. Liver mitochondria from THP-treated rats had increased oxidative metabolism of various substrates and of â -oxidation at 3 weeks, but reduced activities at 6 weeks of THP treatment. Ketogenesis was not affected. The hepatic content of coenzyme A was increased by 23% at 3 and by 40% at 6 weeks in THP treated rats. The cytosolic content of long-chain acyl-CoAs was increased and the mitochondrial content decreased in hepatocytes of THP treated rats, compatible with decreased activity of carnitine palmitoyltransferase I in vivo. THP-treated rats showed hepatic peroxisomal proliferation and increased plasma VLDL triglyceride and phospholipid concentrations at both time points. Conclusions: A reduction in the hepatic carnitine pool is the principle mechanism leading to impaired hepatic fatty acid metabolism and liver steatosis in THP-treated rats. Cytosolic accumulation of long-chain acyl-CoAs is associated with increased plasma VLDL triglyceride and phospholipid concentrations and peroxisomal proliferation. Key words: systemic carnitine deficiency, liver steatosis, mitochondrial and peroxisomal beta-oxidation, peroxisomal proliferation, trimethylhydraziniumpropionate


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