PDF(Pubmed)
Abstract：
In light of the increased worldwide demand for poultry meat, genetic selection efforts have intensified to produce broiler strains that grow at a higher rate, have greater breast meat yield (BMY), and convert feed to meat more efficiently. The increased selection pressure for these traits, BMY in particular, has produced multiple breast meat quality defects collectively known as breast muscle myopathies (BMM). Hypoxia has been proposed as one of the major mechanisms triggering the onset and occurrence of these myopathies. In this review, the relevant literature on the causes and consequences of hypoxia in broiler breast muscles is reviewed and discussed, with a special focus on the hypoxia-inducible factor 1 (HIF-1) pathway. Muscle fiber hypertrophy induced by selective breeding for greater BMY reduces the space available in the perimysium and endomysium for blood vessels and capillaries. The hypoxic state that results from the lack of circulation in muscle tissue activates the HIF-1 pathway. This pathway alters energy metabolism by promoting anaerobic glycolysis, suppressing the tricarboxylic acid cycle and damaging mitochondrial function. These changes lead to oxidative stress that further exacerbate the progression of BMM. In addition, activating the HIF-1 pathway promotes fatty acid synthesis, lipogenesis, and lipid accumulation in myopathic muscle tissue, and interacts with profibrotic growth factors leading to increased deposition of matrix proteins in muscle tissue. By promoting lipidosis and fibrosis, the HIF-1 pathway contributes to the development of the distinctive phenotypes of BMM, including white striations in white striping-affected muscles and the increased hardness of wooden breast-affected muscles.
摘要：
鉴于全球对禽肉的需求增加，基因选择的努力已经加强，以产生生长速度更高的肉鸡菌株，有更高的胸肉产量（BMY），更有效地将饲料转化为肉类。这些性状的选择压力增加，尤其是BMY,产生了多种胸肉质量缺陷，统称为胸肌肌病（BMM）。已经提出缺氧是触发这些肌病的发作和发生的主要机制之一。在这次审查中,对肉鸡胸肌缺氧的原因和后果的相关文献进行了综述和讨论，特别关注缺氧诱导因子1（HIF-1）途径。通过选择性繁殖较大的BMY引起的肌纤维肥大减少了血管和毛细血管的膜周和膜内可用空间。由肌肉组织中循环不足引起的缺氧状态激活HIF-1途径。该途径通过促进无氧糖酵解改变能量代谢，抑制三羧酸循环和破坏线粒体功能。这些变化导致氧化应激，进一步加剧BMM的进展。此外,激活HIF-1途径促进脂肪酸合成，脂肪生成,和肌病肌肉组织中的脂质积累，并与促纤维化生长因子相互作用，导致肌肉组织中基质蛋白的沉积增加。通过促进脂肪沉积和纤维化，HIF-1途径有助于BMM的独特表型的发展，包括白色条纹受影响的肌肉中的白色条纹和木质乳房受影响的肌肉的硬度增加。
