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Sites of Conditional Essential Fatty Acid Deficiency in End Stage Liver Disease
Author(s) -
Burke Peter A.,
Forse Robert A.,
Lewis David W.,
Jenkins Roger,
Bistrian Bruce R.
Publication year - 2001
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607101025004188
Subject(s) - docosahexaenoic acid , polyunsaturated fatty acid , linoleic acid , arachidonic acid , liver disease , medicine , eicosanoid , endocrinology , fatty acid , biochemistry , biology , chemistry , enzyme
Background: End stage liver disease (ESLD) is a devastating illness. Its protean manifestations involve many different aspects of disturbed hepatic function. One consequence of ESLD is a decrease in plasma levels of very long chain polyunsaturated fatty acids (VL‐PUFAs), particularly arachidonic acid (AA) and docosahexaenoic acid (DHA), the former important for eicosanoid metabolism and the latter for retinal and brain membrane structure. The purpose of this study was to define the VL‐PUFA changes in liver disease by comparing plasma and tissue levels of VL‐PUFAs in controls to patients with ESLD. Methods: Fatty acid profiles from plasma, red blood cell (RBC) membranes, muscle, liver, and fat tissue from ESLD patients undergoing liver transplants were measured and compared with control patients undergoing elective liver resection. Results: Fatty acid profiles from plasma and RBC membranes showed significant decreases in AA and DHA levels in patients with ESLD compared with controls. However, there were no significant differences in tissue 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 appear not to be affected by ESLD. Although the mechanism for these changes remains to be defined, it is consistent with hepatic impairment of elongation and desaturation to produce VL‐PUFA for transport. The present results also suggest that dietary interventions to include preformed VL‐PUFA rather than their precursors, linoleic and alpha linolenic acid, would be needed to normalize plasma VL‐PUFA levels in patients with ESLD. (journal of Parenteral and Enteral Nutrition 25:188–193, 2001)