Role of mitochondria in the phenotypic expression of feed efficiency
Role of mitochondria in the phenotypic expression of feed efficiency
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DOI：
10.1093/japr/13.1.94
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发表时间：
2004-03-01
影响因子：
1.9
通讯作者：
Lassiter, K
中科院分区：
文献类型：
--
作者：
Bottje, WG;Iqbal, M;Lassiter, K
最近的研究进行了线粒体获得的低和高饲料效率（FE）的肉鸡在同一遗传系内，喂养相同的饮食，从而允许线粒体功能和FE的表型表达之间的关系，以明确建立。在这些研究中，与低FE肉鸡相比，从高FE肉鸡获得的胸肌、肝脏和十二指肠线粒体显示出更紧密耦合的呼吸链沿着，电子漏和活性氧（ROS）产生更低。在低FE升高的电子泄漏是由于在复合物I，III，或两者的呼吸链在胸部和腿部肌肉和在复合物I，II，或III（取决于能量底物）在十二指肠线粒体的电子传递的位点特异性缺陷。ROS产生的增加可能是低FE肌肉线粒体中蛋白质氧化增加的原因。在研究的14种呼吸链蛋白中，4种（3种在复合体III中，I在复合体IV中）在低FE线粒体中的表达较高。有趣的是，低FE与胸肌和肝脏中呼吸链复合物活性（I，II，III和IV）的一般抑制相关。阐明的机制，负责较低的ROS生产和更紧密的耦合的呼吸链在高FE线粒体将大大有助于我们理解的细胞基础的表型表达FE。
Recent investigations were conducted on mitochondria obtained from broilers with low and high feed efficiency (FE) within the same genetic line that were fed the same diet, thereby allowing relationships between mitochondrial function and the phenotypic expression of FE to be clearly established. In these studies, breast muscle, liver and duodenal mitochondria obtained from broilers with high FE exhibited a more tightly coupled respiratory chain along with lower electron leak and reactive oxygen species (ROS) production compared with broilers with low FE. Elevated electron leak in low FE was due to site-specific defects in electron transport at Complex I, III, or both of the respiratory chains in breast and leg muscles and at Complex I, II, or III (depending on energy substrate) in duodenal mitochondria. Increased ROS production was presumably responsible for increased protein oxidation in low FE muscle mitochondria. Of 14 respiratory chain proteins investigated in breast muscle, the expression of 4 (3 in Complex III and I in Complex IV) was higher in low FE mitochondria. Interestingly, low FE was associated with a general suppression in respiratory chain complex activities (I, II, III, and IV) in breast muscle and liver. Elucidation of the mechanisms responsible for lower ROS production and tighter coupling of the respiratory chain in high FE mitochondria will greatly facilitate our understanding of the cellular basis for the phenotypic expression of FE.