Sites of conditional essential fatty acid deficiency in end stage liver disease

Citation
Pa. Burke et al., Sites of conditional essential fatty acid deficiency in end stage liver disease, J PARENT EN, 25(4), 2001, pp. 188-193
Citations number
21
Categorie Soggetti
Endocrynology, Metabolism & Nutrition
Journal title
JOURNAL OF PARENTERAL AND ENTERAL NUTRITION
ISSN journal
01486071 → ACNP
Volume
25
Issue
4
Year of publication
2001
Pages
188 - 193
Database
ISI
SICI code
0148-6071(200107/08)25:4<188:SOCEFA>2.0.ZU;2-5
Abstract
Background: End stage liver disease (ESLD) is a devastating illness. Its pr otean manifestations involve many different aspects of disturbed hepatic fu nction. One consequence of ESLD is a decrease in plasma levels of very long chain polyunsaturated fatty acids (VL-PUFAs), particularly arachidonic aci d (AA) and docosahexaenoic acid (DHA), the former important for eicosanoid metabolism and the latter for retinal and brain membrane structure. The pur pose of this study was to define the VL-PUFA changes in liver disease by co mparing plasma and tissue levels of VL-PUFAs in controls to patients with E SLD. Methods. Fatty acid profiles from plasma, red blood cell (RBC) membran es, muscle, liver, and fat tissue from ESLD patients undergoing liver trans plants were measured and compared with control patients undergoing elective liver resection. Results: Fatty acid profiles from plasma and RBC membrane s showed significant decreases in AA and DHA levels in patients with ESLD c ompared with controls. However, there were no significant differences in ti ssue fatty acid composition between ESLD patients and controls. Conclusions : ESLD affects the liver's ability to maintain circulating levels of AA and DHA, and thereby presumably RBC membrane levels. However, solid tissues ap pear not to be affected by ESLD. Although the mechanism for these changes r emains to be defined, it is consistent with hepatic impairment of elongatio n and desaturation to produce VL-PUFA for transport. The present results al so suggest that dietary interventions to include preformed VL-PUFA rather t han their precursors, linoleic and alpha linolenic acid, would be needed to normalize plasma VL-PUFA levels in patients with ESLD.