title: Oats (Avena sativa) reduce atherogenesis in LDL-receptor-deficient mice.
abstract: OBJECTIVE
  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.
  
  
  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.
authors.affiliation: Department of Experimental Medical Science, Lund University, Sweden.
authors.forename: K E
authors.initials: KE
authors.lastname: Andersson
authors.forename: K A
authors.initials: KA
authors.lastname: Svedberg
authors.forename: M W
authors.initials: MW
authors.lastname: Lindholm
authors.forename: R
authors.initials: R
authors.lastname: Oste
authors.forename: P
authors.initials: P
authors.lastname: Hellstrand
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D001013:Aorta, Thoracic / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D001018:Aortic Diseases / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D018554:Avena; D001647:Bile Acids and Salts / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D001835:Body Weight; D002784:Cholesterol / Q000097:blood; D004043:Dietary Fiber / Q000008:administration & dosage*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004435:Eating; D005243:Feces / Q000737:chemistry; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D000960:Hypolipidemic Agents / Q000008:administration & dosage*; D018836:Inflammation Mediators / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D051379:Mice; D018345:Mice, Knockout; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D011973:Receptors, LDL / Q000172:deficiency* / Q000235:genetics; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D001647:Bile Acids and Salts; D015415:Biomarkers; D004043:Dietary Fiber; D000960:Hypolipidemic Agents; D018836:Inflammation Mediators; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D011973:Receptors, LDL; D014280:Triglycerides; D019010:Vascular Cell Adhesion Molecule-1; D005340:Fibrinogen; D002784:Cholesterol; D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse