title: Oral supplementation with L-aspartate and L-glutamate inhibits atherogenesis and fatty liver disease in cholesterol-fed rabbit.
abstract: Previous studies have shown that dietary supplementation with L-aspartate and L-glutamate inhibits fatty streak initiation in cholesterol-fed rabbit. The present study investigates the role of dicarboxylic amino acids on the progression of fatty streaks and the development of fatty liver disease, which were caused in New Zealand White rabbits after a 0.5% w/w cholesterol diet for 7 weeks. A group of animals additionally received a combination of 12.5 mM L-aspartate and 12.5 mM L-glutamate per day through drinking water. Total cholesterol (TC), high-density lipoproteins cholesterol (HDLC), non-HDLC and triacylglycerol (TAG) concentrations were measured in plasma. Serum gamma-glutamyl transferase (gamma-GT), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were also determined. At the end of dietary intervention, animals were sacrificed. Aortic, hepatic and brain lesions were evaluated after staining with hematoxylin and eosin. Supplementation with dicarboxylic amino acids inhibited the progression of aortic intima thickness (P < 0.05) and the development of liver lesions (P < 0.05). TC, non-HDLC and TAG were similarly increased in both cholesterol-fed groups. Serum gamma-GT and AST activities elevated during the study in all cholesterol-fed animals but the elevation of gamma-GT was milder and significantly lower in rabbits treated with L-aspartate and L-glutamate (P < 0.05). ALT activity was not affected by cholesterol feeding. In conclusion, oral supplementation with L-aspartate and L-glutamate inhibits the progression of atherogenesis and the development of fatty liver disease in the animal model of cholesterol-fed rabbit. The beneficial effects of dicarboxylic amino acids reflect the limited elevation of serum gamma-GT activity.
authors.affiliation: Department of Dietetics and Nutrition, Harokopio University of Athens, 70 El. Venizelou Avenue, 17671, Athens, Greece. ayanni@hua.gr
authors.forename: Amalia E
authors.initials: AE
authors.lastname: Yanni
authors.forename: George
authors.initials: G
authors.lastname: Agrogiannis
authors.forename: Tzortzis
authors.initials: T
authors.lastname: Nomikos
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Fragopoulou
authors.forename: Alkisti
authors.initials: A
authors.lastname: Pantopoulou
authors.forename: Smaragdi
authors.initials: S
authors.lastname: Antonopoulou
authors.forename: Despoina
authors.initials: D
authors.lastname: Perrea
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001224:Aspartic Acid / Q000008:administration & dosage*; D050197:Atherosclerosis / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000008:administration & dosage*; D005234:Fatty Liver / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D018698:Glutamic Acid / Q000008:administration & dosage*; D008111:Liver Function Tests; D008297:Male; D011817:Rabbits; D014280:Triglycerides / Q000097:blood
chemical_list: D002791:Cholesterol, Dietary; D014280:Triglycerides; D001224:Aspartic Acid; D018698:Glutamic Acid; D002784:Cholesterol