title: Dietary L-aspartate and L-glutamate inhibit fatty streak initiation in cholesterol-fed rabbit.
abstract: OBJECTIVE
  Low-density lipoprotein (LDL) oxidation is a potential atherogenic agent, and protecting LDL from oxidation prevents atherogenesis. It has been shown that L-aspartate and L-glutamate decrease lipid peroxidation after reoxygenation by means of the initiation of the cardiopulmonary bypass circuit (CPB), when supplemented to the CPB prime, and so they may protect against atherogenesis. The aim of this study was to evaluate the effect of the dietary administration of L-aspartate and L-glutamate on fatty streak onset in cholesterol-fed rabbit.
  
  
  RESULTS
  Male New Zealand white rabbits were fed for four weeks with either a high-cholesterol plus corn oil diet (control group) or the same diet supplemented with 12.5 mM L-aspartate and 12.5 mM L-glutamate in drinking water (Asp + Glu group). The mononuclear cells adhering to the endothelium and the intimal foam cells of the thoracic aorta were used to quantify the extent of atherosclerosis. Total serum cholesterol and lipid peroxidation activity, measured as thiobarbituric acid reactive substances (TBARS), were determined 0, 1 and 4 weeks after a 2-week adaptation period. There were no between-group differences in body weight or food intake during the intervention. Serum TBARS were significantly increased in both groups during the experimental period but without any statistical difference between groups. At the end of the dietary intervention, there was a ten-fold increase in total serum cholesterol concentration in both groups vs baseline. The numbers of adherent mononuclear cells and intimal foam cells were both significantly lower in the Asp + Glu group.
  
  
  CONCLUSIONS
  Our results suggest that dietary supplementation with L-aspartate and L-glutamate seems to protect the arterial wall from atherogenesis in an experimental animal.
authors.affiliation: Laboratory of Experimental Surgery and Surgical Research, Medical School, National and Kapodistrian University of Athens, Athens, Greece. ayanni@hua.gr
authors.forename: A E
authors.initials: AE
authors.lastname: Yanni
authors.forename: H A
authors.initials: HA
authors.lastname: Yatzidis
authors.forename: N G
authors.initials: NG
authors.lastname: Kavantzas
authors.forename: E V
authors.initials: EV
authors.lastname: Agapitos
authors.forename: D N
authors.initials: DN
authors.lastname: Perrea
authors.forename: P E
authors.initials: PE
authors.lastname: Karayannacos
mesh_terms: D000818:Animals; D001161:Arteriosclerosis / Q000097:blood / Q000517:prevention & control*; D001224:Aspartic Acid / Q000008:administration & dosage* / Q000494:pharmacology; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000008:administration & dosage*; D004036:Diet, Atherogenic; D004195:Disease Models, Animal; D005487:Foam Cells / Q000378:metabolism; D018698:Glutamic Acid / Q000008:administration & dosage* / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects; D008077:Lipoproteins, LDL / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D010084:Oxidation-Reduction; D011817:Rabbits; D011897:Random Allocation; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D002791:Cholesterol, Dietary; D008077:Lipoproteins, LDL; D017392:Thiobarbituric Acid Reactive Substances; D001224:Aspartic Acid; D018698:Glutamic Acid; D002784:Cholesterol