| DHA supplemented in peptamen diet offers no advantage in pathways to amyloidosis: is it time to evaluate composite lipid diet? | |
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MedLine Citation:
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PMID: 21931647 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Numerous reports have documented the beneficial effects of dietary docosahexaenoic acid (DHA) on beta-amyloid production and Alzheimer's disease (AD). However, none of these studies have examined and compared DHA, in combination with other dietary nutrients, for its effects on plaque pathogenesis. Potential interactions of DHA with other dietary nutrients and fatty acids are conventionally ignored. Here we investigated DHA with two dietary regimes; peptamen (pep+DHA) and low fat diet (low fat+DHA). Peptamen base liquid diet is a standard sole-source nutrition for patients with gastrointestinal dysfunction. Here we demonstrate that a robust AD transgenic mouse model shows an increased tendency to produce beta-amyloid peptides and amyloid plaques when fed a pep+DHA diet. The increase in beta-amyloid peptides was due to an elevated trend in the levels of beta-secretase amyloid precursor protein (APP) cleaving enzyme (BACE), the proteolytic C-terminal fragment beta of APP and reduced levels of insulin degrading enzyme that endoproteolyse beta-amyloid. On the contrary, TgCRND8 mice on low fat+DHA diet (based on an approximately 18% reduction of fat intake) ameliorate the production of abeta peptides and consequently amyloid plaques. Our work not only demonstrates that DHA when taken with peptamen may have a tendency to confer a detrimental affect on the amyloid plaque build up but also reinforces the importance of studying composite lipids or nutrients rather than single lipids or nutrients for their effects on pathways important to plaque development. |
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Authors:
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Zareen Amtul; Mary Keet; Lin Wang; Peter Merrifield; David Westaway; Richard F Rozmahel |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-09-08 |
Journal Detail:
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Title: PloS one Volume: 6 ISSN: 1932-6203 ISO Abbreviation: PLoS ONE Publication Date: 2011 |
Date Detail:
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Created Date: 2011-09-20 Completed Date: 2012-03-01 Revised Date: 2012-04-26 |
Medline Journal Info:
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Nlm Unique ID: 101285081 Medline TA: PLoS One Country: United States |
Other Details:
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Languages: eng Pagination: e24094 Citation Subset: IM |
Affiliation:
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Department of Biochemistry, University of Western Ontario, London, Ontario, Canada. zamtul@uwo.ca |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Alzheimer Disease
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metabolism,
pathology Amyloid Precursor Protein Secretases / metabolism Amyloid beta-Peptides / genetics, metabolism Amyloid beta-Protein Precursor / genetics, metabolism Amyloidosis / metabolism*, pathology, prevention & control Animals Aspartic Acid Endopeptidases / metabolism Brain / drug effects, metabolism, pathology Diet* Dietary Fats / administration & dosage Dietary Supplements Docosahexaenoic Acids / administration & dosage* Down-Regulation / drug effects Fatty Acids / metabolism Gene Expression / drug effects Immunohistochemistry Insulysin / metabolism Mice Mice, Transgenic Oligopeptides / administration & dosage* Plaque, Amyloid / metabolism Reverse Transcriptase Polymerase Chain Reaction Up-Regulation / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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MOP49546//Canadian Institutes of Health Research |
| Chemical | |
Reg. No./Substance:
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0/Amyloid beta-Peptides; 0/Amyloid beta-Protein Precursor; 0/Dietary Fats; 0/Fatty Acids; 0/Oligopeptides; 0/Peptamen; 25167-62-8/Docosahexaenoic Acids; EC 3.4.-/Amyloid Precursor Protein Secretases; EC 3.4.23.-/Aspartic Acid Endopeptidases; EC 3.4.23.46/BACE1 protein, human; EC 3.4.24.56/Insulysin |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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