Vitamin A deficiency modifies lipid metabolism in rat liver.
Liver fatty acid metabolism of male rats fed on a vitamin A-deficient diet for 3 months from 21 d of age was evaluated. Vitamin A restriction produced subclinical plasma and negligible liver retinol concentrations, compared with the control group receiving the same diet with 4000 IU vitamin A (8 mg retinol as retinyl palmitate)/kg diet. Vitamin A deficiency induced a hypolipidaemic effect by decreasing serum triacylglycerol, cholesterol and HDL-cholesterol levels. The decrease of liver total phospholipid was associated with low phosphatidylcholine synthesis observed by lower [14C]choline incorporation into phosphatidylcholine, compared with control. Also, liver fatty acid synthesis decreased, as was indicated by activity and mRNA expression of acetyl-CoA carboxylase (ACC), and incorporation of [14C]acetate into saponified lipids. A decrease of the PPARalpha mRNA expression was observed. Liver mitochondria of vitamin A-deficient rats showed a lower total phospholipid concentration coinciding with a decrease of the cardiolipin proportion, without changes in the other phospholipid fractions determined. The mitochondria fatty acid oxidation increased by 30 % of the control value and it was attributed to a high activity and mRNA expression of carnitine palmitoyltransferase-I (CPT-I). An increase in serum beta-hydroxybutyrate levels was observed in vitamin A-deficient rats. Vitamin A deficiency alters the mitochondria lipid composition and also enhances fatty acid oxidation by modifying the production of malonyl-CoA, the endogenous inhibitor of CPT-I, due to decreased activity of liver ACC. The incorporation of vitamin A into the diet of vitamin A-deficient rats reverted all the changes observed.
Oliveros
Liliana B
LB
Laboratory of Biological Chemistry, Faculty of Chemistry, Biochemistry and Pharmacy, National University of San Luis, Avenida Ejército de los Andes 954, 5700 San Luis, Argentina.
Domeniconi
María A
MA
Vega
Verónica A
VA
Gatica
Laura V
LV
Brigada
Ana M
AM
Gimenez
María S
MS
D000103:Acetyl-CoA Carboxylase / Q000032:analysis / Q000378:metabolism; D000818:Animals; D001835:Body Weight / Q000502:physiology; D002334:Carnitine O-Palmitoyltransferase / Q000032:analysis / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D004032:Diet; D005227:Fatty Acids / Q000378:metabolism; D050356:Lipid Metabolism / Q000502:physiology*; D008055:Lipids / Q000097:blood; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism; D009929:Organ Size / Q000502:physiology; D010084:Oxidation-Reduction; D047493:PPAR alpha / Q000032:analysis; D010713:Phosphatidylcholines / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013109:Sphingomyelins / Q000378:metabolism; D014801:Vitamin A / Q000097:blood; D014802:Vitamin A Deficiency / Q000378:metabolism*
D005227:Fatty Acids; D008055:Lipids; D047493:PPAR alpha; D010713:Phosphatidylcholines; D012333:RNA, Messenger; D013109:Sphingomyelins; D014801:Vitamin A; D002784:Cholesterol; D002334:Carnitine O-Palmitoyltransferase; D000103:Acetyl-CoA Carboxylase