北京油鸡AMPK基因表达规律及其对肌肉和脂肪细胞内脂肪沉积的影响

The Expression of Beijing-You Chicken AMPK Gene and Its Effects on the Adipogenesis in the Muscle and Adipocyte

本研究旨在揭示一磷酸腺苷激活蛋白酶(AMPK)基因在北京油鸡(BJY)腿肌中的表达规律及其在肌内脂肪(IMF)沉积的中的作用。选择体质量一致的1日龄北京油鸡(BJY)90只,随机分为6组,每组15只,饲养于标准鸡舍,饲养过程自由采食和饮水,在相同营养标准和管理条件下饲养至1、56、112日龄进行屠宰,测定腿肌AMPK各亚基基因和脂肪代谢基因表达水平与肌内脂肪的含量,通过计算2-ΔΔCT值来衡量不同阶段基因相对表达量的差异。研究结果表明,BJY鸡腿肌AMPKα2和AMPKγ2基因在56日龄的表达量低于1(P>0.05)和112日龄(P<0.05)的表达量,与腿肌肌内脂肪(IMF)含量及过氧化物酶体增殖物激活受体(PPAR)α和γ、脂肪酸转位酶CD36(FAT/CD36)、脂肪酸合成酶(FAS)、Ca信号受体(CASR)等基因表达量的变化趋势一致;而AMPKβ1、AMPKβ2和AMPKγ1基因的56日龄表达量高于1(P<0.05)和112日龄(P>0.05)的表达量,与腿肌肌内脂肪含量及脂肪代谢基因(PPARα、PPARγ、FAT、FAS、CASR)的变化呈相反趋势。细胞培养研究表明,前体脂肪细胞经过AMPK激活剂AICAR处理后,细胞脂质蓄积能力和PPARα、PPARγ基因表达有所降低,而经过抑制剂Compound C处理后,细胞脂质蓄积能力和PPARα、PPARγ基因表达会增加。这些结果表明AMPK对脂肪细胞的脂质蓄积有一定的抑制作用。因此,AMPK基因对肌内脂肪沉积具有一定调控作用,特别是AMPKβ1、AMPKβ2和AMPKγ1基因具有显著的负调控作用。

The objective of the study was to explore the expression of adenosine monophosphateactivated protein kinase （AMPK） in the BJY chicken thigh muscle and its effects on the intramuscular fat（IMF）. The BJY chickens were divided randomly into 6 treatments and 15 chickens each treatment. The chickens were fed under the same feeding standards and management condition. The chickens were slaughtered on the 1, 56, 112 days old and the expression of AMPK and lipid metabolic gene and IMF contents of thigh muscle were measured. The difference of gene expression was calculated by the method of of 2- ΔΔCT value. The results showed that the expression levels of AMPKα2 and AMPKγ2 genes on the 56 days old in BJY chickens were lower than that on 1 （P〉0.05） and 112 days old （P〈0.05）, which had the same trend with the gene expression of peroxisome proliferator activated receptor（PPAR）α and γ, Fatty Acid Translocase CD36 （FAT/CD36）, Fatty acid synthase （FAS）, Calciumsensing receptor （CASR）. But the expression of AMPKβ1, AMPKβ2 and AMPKγ1 on the 56 days old were higher than that on 1 （P〈0.05） and 112 days old （P〉0.05）, which had inverse trend with the expression of lipid metabolic genes （PPARα, PPARγ, FAT, FAS, CASR）. The results of the study on cell incubation showed that the activation of AMPK by AICAR inhibited the expression of PPARα and PPARγ and reduced the lipid accumulation in preadipocyte. But inhibition of AMPK by compound C enhanced the expression of PPARα and PPARγ and promoted the lipid accumulation in preadipocyte. In conclusion, these data show that AMPK, especially AMPKβ1, AMPKβ2 and AMPKγ1, may play a negative regulation role in the process of adipogenesis.