Role Of PPARs And Its Target Genes In Estrogen-induced Fatty Liver Hemorrhagic Syndrome In Laying Hens

Two experiments were conducted to study the role of PPARs and its target genes inestrogen-induced fatty liver hemorrhagic syndrome (FLHS) in laying hens. Firstly, FLHS was inducedin laying hens by estrogen injection and the correlation between PPARs and FLHS was investigated byexaming the mRNA expression of PPARs and its target genes. The second experiment was conducted toinvestigate that if choline chloride can inhibite FLHS induced by estrogen. Data of the two experimentsindicated the role of PPARs and its target genes in estrogen-induced FLHS in laying hens.Experiment1The role of PPARs and its target genes in estrogen-induced FLHS in laying hensIn this test, a total of20Hy-line Brown hens were divided into two groups with10replicatesaccording to the body weight and egg production rates. The treated group was injected β-estradiol withthe dose of7.5mg β-estradiol/0.5mL corn oil/kg BW, and the control group was injected with0.5mLcorn oil/kg BW. It was injected every three days for five times. The results showed that the liver fatcontent and liver hemorrhagic indexes in treated group were significant higher than in control group,and the incidence of FLHS in treated group was70%, which suggested that FLHS was induced byβ-estradiol successfully.After the development of FLHS, the mRNA expression of PPARs and its target genes wereinvestigated by RT-PCR(reverse transcription polymerase chain reaction) to study the role of PPARs andits target genes(3-hydroxy-3-methyl glutaryl coenzyme A synthetase, Acyl-coa Oxidase, adipocyte-fattyacid binding protein, Fatty acid transport enzymes) in estrogen-induced FLHS in laying hens. Theresults showed that the mRNA expression of PPARα in treated group was lower than control group,while the mRNA expression of HMG-CoAS and PPARγ was significant higher than in control group（P<0.05). There were no significant difference in the mRNA expression of PPARβ、ACOX、AFABP�'�FAT（P>0.05). It suggested that β-estradiol can induce FLHS by increasing the mRNAexpression ofHMG-CoAS and PPARγ.Experiment2the role of PPARs and its target genes in estrogen-induced FLHS by choline chlorideadministrationThis test was conducted to invesitigate the mRNA expression of PPARs and its target genes inFLHS with injection of choline chloride. A total of120Hy-line Brown hens were divided into fourgroups with15replicates according to the body weight and egg production rates. Chickens in controlgroup were injected with normal saline, the treated groups were injected with β-estradiol, cholinechloride, respectively. It was injected every three days for five times. By investigating the mRNAexpression of PPARs and its target genes in liver, the important effects of PPARs and its target genes inFLHS induced by estrogen can be confirmed. The results showed that the incidence of FLHS in groupⅢ and group Ⅳ was68.97%and67.86%, which was higher than in control group (10.34%) and groupⅡ(0%), it suggested that the administration of choline chloride can definitly inhibite FLHS. The mRNA expression of PPARα in group Ⅲ and group Ⅳ was lower than in control group and group Ⅱ（P>0.05), the mRNA expression of HMG-CoAS and PPARγ was significant higher than in controlgroup and group Ⅱ（P<0.05). The mRNA expression of AFABP in group Ⅳ was significant higher thanin control group（P<0.05).There were no significant difference in the mRNA expression of PPARs andits target genes neither in group Ⅱand control group nor in group Ⅲ and group Ⅳ. It suggested that theinhibition of choline chloride to FLHS was not through the effect of PPARs and its target genes.The research showed that FLHS can be induced by β-estradiol; HMG-CoAS and PPARγplay animportant role in the development of FLHS induced by β-estradiol; FLHS can definitly be inhibited byCholine chloride, while it was not through the mRNA expression of PPARs and its target genes.