Alterations in the lipid metabolism of rat aorta: effects of vitamin a deficiency.
Antioxidants are known to reduce cardiovascular disease by reducing the concentration of free radicals in the vessel wall and by preventing the oxidative modification of low-density lipoproteins. The prooxidative effect of a vitamin-A-deficient diet on the aorta has previously been demonstrated by us. In this study, the lipid metabolism in the aorta of rats fed on a vitamin-A-deficient diet was evaluated. Vitamin A deficiency induced a hypolipidemic effect (lower serum triglyceride and cholesterol levels) and a decreased serum paraoxonase 1/arylesterase activity. The concentrations of triglycerides, total cholesterol, free and esterified cholesterol, and phospholipids were increased in the aorta of vitamin-A-deficient rats. The phospholipid compositions showed an increase in phosphatidylcholine (PC), phosphatidylinositol plus phosphatidylserine and phosphatidylethanolamine, a decrease in sphingomyelin, and no change in phosphatidylglycerol. In the aorta, the increase in triglycerides was associated with an increased fatty acid synthesis and mRNA expression of diacylglycerol acyltransferase 1. The increased PC content was attributed to an increased synthesis, as measured by [methyl-(14)C]choline incorporation into PC and high CTP:phosphocholine cytidylyltransferase-alpha mRNA expression. The cholesterol synthesis, evaluated by [1-(14)C]acetate incorporated into cholesterol and mRNA expression of 3-hydroxy-3-methylglutaryl coenzyme A reductase, did not change. The lipoprotein lipase and lectin-like oxidized low-density lipoprotein receptor 1 mRNA expression levels increased in the aorta of vitamin-A-deficient animals. The incorporation of vitamin A into the diet of vitamin-A-deficient rats reverted all the changes observed. These results indicate that a vitamin-A-deficient diet,in addition to having a prooxidative effect, alters the aorta lipid metabolism.
Gatica
Laura V
LV
Department of Biochemistry and Biological Sciences, Faculty of Chemistry, Biochemistry and Pharmacy, National University of San Luis, San Luis, Argentina.
Vega
Verónica A
VA
Zirulnik
Fanny
F
Oliveros
Liliana B
LB
Gimenez
María S
MS
D000085:Acetates / Q000493:pharmacokinetics; D000818:Animals; D001011:Aorta / Q000378:metabolism*; D043303:Aryldialkylphosphatase / Q000097:blood / Q000235:genetics; D001835:Body Weight; D002250:Carbon Radioisotopes; D002784:Cholesterol / Q000096:biosynthesis; D008076:Cholesterol, HDL / Q000097:blood; D002794:Choline / Q000493:pharmacokinetics; D019916:Choline-Phosphate Cytidylyltransferase / Q000235:genetics; D051048:Diacylglycerol O-Acyltransferase / Q000235:genetics; D005227:Fatty Acids / Q000096:biosynthesis; D006903:Hydroxymethylglutaryl CoA Reductases / Q000235:genetics; D050356:Lipid Metabolism / Q000502:physiology*; D008297:Male; D010713:Phosphatidylcholines / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D051127:Scavenger Receptors, Class E / Q000235:genetics; D013109:Sphingomyelins / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D014801:Vitamin A / Q000097:blood; D014802:Vitamin A Deficiency / Q000378:metabolism* / Q000503:physiopathology
D000085:Acetates; D002250:Carbon Radioisotopes; D008076:Cholesterol, HDL; D005227:Fatty Acids; C495136:OLR1 protein, rat; D010713:Phosphatidylcholines; D012333:RNA, Messenger; D051127:Scavenger Receptors, Class E; D013109:Sphingomyelins; D014280:Triglycerides; D014801:Vitamin A; D002784:Cholesterol; D006903:Hydroxymethylglutaryl CoA Reductases; C494883:Dgat1 protein, rat; D051048:Diacylglycerol O-Acyltransferase; D019916:Choline-Phosphate Cytidylyltransferase; D043303:Aryldialkylphosphatase; D002794:Choline