Abstract
Vitamin A (VA) deficiency is still a major health problem in the developing world. It affects various cellular functions and causes hypolipidemic effects in the body. β-Carotene (BC)-rich foods are promising sources of VA. Phospholipids are reported to improve BC bioefficacy in normal rats, but whether they show similar effects during VA deficiency is unknown. To compare the BC metabolism and plasma lipid responses in VA-sufficient (+VA) and VA-deficient (-VA) rats after a single oral dose of micellar BC containing phospholipids. Groups of rats were fed with a VA-free diet and when they attained the weight-plateau stage of deficiency, both +VA and -VA rats were divided into 2 groups (phosphatidylcholine, PC and lysophosphatidylcholine, LPC). Each group was further divided into 4 subgroups (1, 2, 3, and 6 h; n = 5 rats/time point) and determined the BC metabolism and plasma lipid responses to a post-dose of micellar BC with phospholipids. Maximal plasma BC (pmol/mL) levels were observed at 2 h in PC (1330 ± 124) and at 1 h in LPC (1576 ± 144) groups of +VA rats, and at 3 h in the PC (1621 ± 158) and LPC (2248 ± 675) groups of -VA rats. Liver BC (pmol/g) was maximum at 1 h in the PC (218 ± 32) and LPC (249 ± 24) groups of +VA rats, and at 2 h in PC (228 ± 23) and at 3 h in LPC (277 ± 18) groups of -VA rats. Plasma and liver BC levels were significantly (P < 0.05) higher in -VA rats than +VA rats. Plasma retinyl palmitate (pmol/mL) was maximum at 3 h in PC (97 ± 18) and at 2 h in LPC (126 ± 14) groups of +VA rats, and at 2 h in the PC (92 ± 13) and LPC (134 ± 27) groups of -VA rats. The higher (P < 0.05) BC monoxygenase activity in -VA rats compared to +VA rats supports the BC bioefficacy. Plasma retinol level was improved in the PC and LPC groups, but the effect of LPC was higher (P < 0.05) than PC. Micellar phospholipids mitigate the VA deficiency-induced hypolipidemic effects. Micellar phospholipids improved BC metabolism and reinstated the hypolipidemic effects, perhaps by modifying the fat-metabolizing enzymes and repairing the altered intestinal membrane structure.
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