title: Nutritional B vitamin deficiency disrupts lipid metabolism causing accumulation of proatherogenic lipoproteins in the aorta adventitia of ApoE null mice.
abstract: METHODS
  Cardiovascular disease is the major cause of death in the world. Low dietary folate, elevated homocysteine, and high circulating cholesterol are risk factors.
  
  
  RESULTS
  We investigated whether folate and/or B vitamin deficiency would change lipoprotein and fatty acid metabolism and lipid accumulation in the aorta adventitia of ApoE null mice. Mice (n = 10 per group) were fed a control (C; 4%) or high saturated fat (HF; 21%), and high cholesterol (0.15%) diet for 16 weeks. Folate (F-) or folate, B6 and B12 deficiency (F-B-) were imposed on these diets. Feeding a HF diet increased plasma and liver total cholesterol and HDL cholesterol (two- to threefold; p < 0.05). Total cholesterol increased (twofold; p < 0.05) in aorta adventitial lipid in response to HF. Feeding a diet depleted of folate and B vitamins (F-B-) significantly increased cholesterol accumulation in both liver and aorta adventitial lipid (approximately 50-70%; p < 0.05). Moreover, the proportions of fatty acids in hepatic and adventitial lipid was significantly changed by B vitamin depletion, measured as an increase in saturated fatty acids (approximately 15%) and a decrease (approximately 11%) in monounsaturated fatty acids (p < 0.05).
  
  
  CONCLUSIONS
  B vitamin deficiency perturbs lipid metabolism in ApoE null mice, causing accumulation of proatherogenic cholesterol and fatty acids in the aorta adventitia.
authors.affiliation: Division of Lifelong Health, Rowett Institute of Nutrition and Health, University of Aberdeen, Aberdeen, United Kingdom.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: McNeil
authors.forename: John H
authors.initials: JH
authors.lastname: Beattie
authors.forename: Margaret-Jane
authors.initials: MJ
authors.lastname: Gordon
authors.forename: Lynn P
authors.initials: LP
authors.lastname: Pirie
authors.forename: Susan J
authors.initials: SJ
authors.lastname: Duthie
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism*; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D003238:Connective Tissue / Q000378:metabolism*; D004036:Diet, Atherogenic / Q000009:adverse effects; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000097:blood / Q000378:metabolism; D020138:Hyperhomocysteinemia / Q000209:etiology; D050356:Lipid Metabolism; D008074:Lipoproteins / Q000097:blood / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D012435:S-Adenosylhomocysteine / Q000378:metabolism; D012436:S-Adenosylmethionine / Q000378:metabolism; D012720:Severity of Illness Index; D014804:Vitamin B Deficiency / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D001057:Apolipoproteins E; D005227:Fatty Acids; D008074:Lipoproteins; D012436:S-Adenosylmethionine; D012435:S-Adenosylhomocysteine; D002784:Cholesterol