Docosahexaenoic Acid and Arachidonic Acid Prevent Essential Fatty Acid Deficiency and Hepatic Steatosis
Objectives: Essential fatty acids are important for growth, development, and physiologic function. α-Linolenic acid and linoleic acid are the precursors of docosahexaenoic and arachidonic acid, respectively, and have traditionally been considered the essential fatty acids. However, the authors hypot...
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Published in: | JPEN. Journal of parenteral and enteral nutrition Vol. 36; no. 4; pp. 431 - 441 |
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Main Authors: | , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Los Angeles, CA
SAGE Publications
01-07-2012
Sage Publications |
Subjects: | |
Online Access: | Get full text |
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Summary: | Objectives: Essential fatty acids are important for growth, development, and physiologic function. α-Linolenic acid and linoleic acid are the precursors of docosahexaenoic and arachidonic acid, respectively, and have traditionally been considered the essential fatty acids. However, the authors hypothesized that docosahexaenoic acid and arachidonic acid can function as the essential fatty acids. Methods: Using a murine model of essential fatty acid deficiency and consequent hepatic steatosis, the authors provided mice with varying amounts of docosahexaenoic and arachidonic acids to determine whether exclusive supplementation of docosahexaenoic and arachidonic acids could prevent essential fatty acid deficiency and inhibit or attenuate hepatic steatosis. Results: Mice supplemented with docosahexaenoic and arachidonic acids at 2.1% or 4.2% of their calories for 19 days had normal liver histology and no biochemical evidence of essential fatty acid deficiency, which persisted when observed after 9 weeks. Conclusion: Supplementation of sufficient amounts of docosahexaenoic and arachidonic acids alone without α-linolenic and linoleic acids meets essential fatty acid requirements and prevents hepatic steatosis in a murine model. |
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Bibliography: | Financial disclosure: HDL and EMF were recipients of the Joshua Ryan Rappaport Fellowship. EMF was supported by the National Institute of Diabetes and Digestive and Kidney Diseases (F32DK083880). MP was supported by the National Institutes of Health (DK069621‐05). HDL, JAM, VEM, EMF, and MP were supported by the Children's Hospital Surgical Foundation and the Vascular Biology Program (Boston, MA). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0148-6071 1941-2444 0148-6071 |
DOI: | 10.1177/0148607111414580 |