| Oats (Avena sativa) reduce atherogenesis in LDL-receptor-deficient mice. | |
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MedLine Citation:
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PMID: 20553794 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIM: The cholesterol-lowering properties of oats, largely ascribed to its contents of soluble fibers, beta-glucans, are well established, whereas effects on atherogenesis are less well elucidated. Oats also contains components with reported antioxidant and anti-inflammatory effects that may affect atherogenesis. In this work we examined effects of oat bran on plasma cholesterol, markers of inflammation, eNOS expression and development of atherosclerosis in LDL-receptor-deficient (LDLr(-/-)) mice. METHODS AND RESULTS: Female LDLr(-/-) mice were fed Western diet+/-oat bran. Two concentrations of oat bran (40 and 27%) were compared regarding effects on plasma lipids. There was a dose-dependent reduction of plasma cholesterol by 42 and 20% with 40 and 27% oat bran, respectively. Both concentrations also lowered plasma triglycerides (by 45 and 33%) and relative levels of plasma LDL+VLDL. The reduction of plasma lipids was accompanied by increased faecal excretion of cholesterol and bile acids. Oat bran (40%) efficiently reduced atherosclerotic lesion area in the descending aorta (-77%) and aortic root (-33%). Plasma levels of fibrinogen and soluble vascular cell adhesion molecule-1 (VCAM-1) were significantly lower, and immunofluorescence of aortic sections revealed a 75% lower expression of VCAM-1 in oat-fed mice. The expression of eNOS protein in the aortic wall was increased in mice fed oat bran. CONCLUSIONS: Oat bran supplemented to a Western diet lowers plasma cholesterol, reduces levels of some inflammatory markers, increases eNOS expression and inhibits atherosclerotic lesion development in LDLr(-/-) mice. It remains to be investigated which components in oats contribute to these effects. |
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Authors:
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K E Andersson; K A Svedberg; M W Lindholm; R Oste; P Hellstrand |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-05-11 |
Journal Detail:
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Title: Atherosclerosis Volume: 212 ISSN: 1879-1484 ISO Abbreviation: Atherosclerosis Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-03 Completed Date: 2010-12-28 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0242543 Medline TA: Atherosclerosis Country: Ireland |
Other Details:
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Languages: eng Pagination: 93-9 Citation Subset: IM |
Copyright Information:
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Copyright 2010 Elsevier Ireland Ltd. All rights reserved. |
Affiliation:
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Department of Experimental Medical Science, Lund University, Sweden. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anti-Inflammatory Agents / administration & dosage* Aorta, Thoracic / drug effects, enzymology, pathology Aortic Diseases / genetics, metabolism, pathology, prevention & control* Atherosclerosis / genetics, metabolism, pathology, prevention & control* Avena sativa* Bile Acids and Salts / metabolism Biological Markers / blood Body Weight Cholesterol / blood Dietary Fiber / administration & dosage* Disease Models, Animal Dose-Response Relationship, Drug Eating Feces / chemistry Female Fibrinogen / metabolism Hypolipidemic Agents / administration & dosage* Inflammation Mediators / blood Lipoproteins, LDL / blood Lipoproteins, VLDL / blood Mice Mice, Knockout Nitric Oxide Synthase Type III / metabolism Receptors, LDL / deficiency*, genetics Time Factors Triglycerides / blood Vascular Cell Adhesion Molecule-1 / blood |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents; 0/Bile Acids and Salts; 0/Biological Markers; 0/Hypolipidemic Agents; 0/Inflammation Mediators; 0/Lipoproteins, LDL; 0/Lipoproteins, VLDL; 0/Receptors, LDL; 0/Triglycerides; 0/Vascular Cell Adhesion Molecule-1; 57-88-5/Cholesterol; 9001-32-5/Fibrinogen; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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