title: A casein variant in cow's milk is atherogenic.
abstract: Casein is a major protein in cow's milk that occurs in several variant forms, two of which are beta-casein A1 and beta-casein A2. The levels of these two proteins vary considerably in milk dependent on the breed of cow, and epidemiology studies suggest that there is a relationship between their consumption and the degree of atherosclerosis. In the present study, the direct effect of consumption of beta-casein A1 vs beta-casein A2 on atherosclerosis development was examined in a rabbit model. Sixty rabbits had their right carotid artery balloon de-endothelialised at t=0, divided randomly into 10 groups (n=6 per group), then for 6 weeks fed a diet containing 0, 5, 10 or 20% casein isolate, either beta-casein variant A1 or A2, made up to 20% milk protein with whey. Some groups had their diets supplemented with 0.5% cholesterol. Blood samples were collected at t=0, 3 and 6 weeks and rabbits were sacrificed at t=6 weeks. In the absence of dietary cholesterol, beta-casein A1 produced significantly higher (P<0.05) serum cholesterol, LDL, HDL and triglyceride levels than whey diet alone, which in turn produced higher levels than beta-casein A2. Rabbits fed beta-casein A1 had a higher percent surface area of aorta covered by fatty streaks than those fed beta-casein A2 (5.2+/-0.81 vs 1.1+/-0.39, P<0.05) and the thickness of the fatty streak lesions in the aortic arch was significantly higher (0.04+/-0.010 vs 0.00, P<0.05). Similarly, the intima to media ratio (I:M) of the balloon injured carotid arteries in A1 fed animals (0.77+/-0.07) was higher than in those that consumed A2 (0.57+/-0.04) or whey (0.58+/-0.04), but this did not reach significance. In the presence of 0.5% dietary cholesterol, the thickness of the aortic arch lesions was higher (P<0.05) in 5, 10 and 20% casein A1 fed animals compared with their A2 counterparts, while other parameters were not significantly different. It is concluded that beta-casein A1 is atherogenic compared with beta-casein A2.
authors.affiliation: Centre for Research in Vascular Biology, School of Biomedical Sciences, University of Queensland, Brisbane, Qld 4072, Australia.
authors.forename: Kristy A
authors.initials: KA
authors.lastname: Tailford
authors.forename: Celia L
authors.initials: CL
authors.lastname: Berry
authors.forename: Anita C
authors.initials: AC
authors.lastname: Thomas
authors.forename: Julie H
authors.initials: JH
authors.lastname: Campbell
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000378:metabolism; D001013:Aorta, Thoracic / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D002340:Carotid Artery Diseases / Q000378:metabolism; D002343:Carotid Artery, Internal / Q000378:metabolism / Q000473:pathology; D002364:Caseins / Q000008:administration & dosage* / Q000235:genetics* / Q000378:metabolism; D002614:Chelating Agents / Q000008:administration & dosage* / Q000378:metabolism*; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004036:Diet, Atherogenic; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D014644:Genetic Variation; D006710:Homocysteine / Q000097:blood; D008297:Male; D008892:Milk / Q000737:chemistry* / Q000378:metabolism*; D008955:Models, Cardiovascular; D010865:Pilot Projects; D011817:Rabbits; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D017539:Tunica Intima / Q000378:metabolism / Q000473:pathology; D015431:Weight Loss
chemical_list: D015415:Biomarkers; D002364:Caseins; D002614:Chelating Agents; D002791:Cholesterol, Dietary; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; D006710:Homocysteine