Objective   To study the effect of vitamin A deficiency (VAD) on lipid metabolism in a rat kidney model and its related molecular mechanism.  Methods   Wistar rats were divided into normal control group (n=6)

VAD group (n=6)

and vitamin A supplement (VAS) group (n=6). Rats in normal control group were fed with a diet containing 4 000 IU/kg of vitamin A

rats in VAD group were fed with a diet containing 400 IU/kg of vitamin A

and rats in VAS group were fed with a diet containing 400 IU/kg of vitamin A for 8 weeks followed by a diet containing 6 500 IU/kg of vitamin A for 15 d. Apolipoprotein B100 (Apo-B100) was analyzed with immunohistochemistry. Expression levels of adenosine triphosphate (ATP) binding cassette A1 (ABCA1) in kidneys

peroxime proliferator activated receptor α (PPARα)

liver X receptor α (LXRα)

and retinoid X receptor-α/β (RXRα/β) mRNA were measured by real-time PCR.  Results   Immunohistochemistry analysis showed that the Apo-B100 expression level was significantly higher in VAD group than in normal control group（14.27±0.05 vs 8.25±0.49

P0.05）while expression level of ABCA1 was significantly lower in VAD group than in normal control group 8 weeks after treatment with vitamin A（24.53±0.86 vs 37.44±0.46

P0.05）. Real-time PCR showed that the expression level of ABCA1 was higher and the expression level of LXRα

RXRα/β mRNA was lower in VAD group than in normal control group (P0.05). No difference was found in expression of ABCA1 and LXRα

RXRα/β mRNA between the two groups. The above changes returned to their normal level after treatment with vitamin A.  Conclusion  VAD can lead to ABCA1-mediated lipid efflux pathway injury of PPARα/RXRs-LXRα/RXRs

resulting in lipid accumulation in rat kidneys

which would return to its normal level after treatment with vitamin A.