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Am J Physiol Gastrointest Liver Physiol 279: G1242-G1248, 2000;
0193-1857/00 $5.00
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Vol. 279, Issue 6, G1242-G1248, December 2000

Intestinal absorption and postabsorptive metabolism of linoleic acid in rats with short-term bile duct ligation

Deanna M. Minich, Rick Havinga, Frans Stellaard, Roel J. Vonk, Folkert Kuipers, and Henkjan J. Verkade

Institute for Liver, Digestive, and Metabolic Diseases, Department of Pediatrics, University Hospital Groningen, 9700 RB Groningen, The Netherlands

We investigated in bile duct-ligated (BDL) and sham-operated control rats whether the frequent presence of essential fatty acid deficiency in cholestatic liver disease could be related to linoleic acid malabsorption, altered linoleic acid metabolism, or both. In plasma of BDL rats, the triene-to-tetraene ratio, a biochemical marker for essential fatty acid deficiency, was increased compared with controls (0.024 ± 0.004 vs. 0.013 ± 0.001; P < 0.05). Net and percentage of dietary linoleic acid absorbed were decreased in BDL rats compared with control rats (1.50 ± 0.16 mmol/day and 81.3 ± 3.3% vs. 2.08 ± 0.07 mmol/day and 99.2 ± 0.1%, respectively; each P < 0.001). At 24 h after [13C]linoleic acid administration, BDL rats had a similar ratio of plasma [13C]arachidonic acid to plasma [13C]linoleic acid concentration compared with control rats. Delta 6-Desaturase activity was not significantly different in hepatic microsomes from control or BDL rats. At 3 h after [13C]linoleic acid administration, plasma appearance of [13C]linoleic acid and cumulative expiration of 13CO2 were decreased in BDL rats, compared with controls (by 54% and 80%, respectively). The present data indicate that the impaired linoleic acid status in cholestatic liver disease is mainly due to decreased net absorption and not to quantitative alterations in postabsorptive metabolism.

essential fatty acid; enterohepatic circulation; cholestasis; stable isotope


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