Department of Animal Science, National Chung Hsing University, Taichung, Taiwan.
Department of Poultry Science, Texas A&M University, College Station.
Poult Sci. 2017 Jul 1;96(7):2438-2446. doi: 10.3382/ps/pex016.
Feed intake is typically restricted (R) in broiler hens to avoid obesity and improve egg production and livability. To determine whether improved heart health contributes to improved livability, fully adult 45-week-old R hens were allowed to consume feed to appetite (ad libitum; AL) up to 10 wk (70 d). Mortality, contractile functions, and morphology at 70 d, and measurements of cardiac hypertrophic remodeling at 7 d and 21 d were made and compared between R and AL hens. Outcomes for cardiac electrophysiology and mortality, reported separately, found increased mortality in AL hens in association with cardiac pathological hypertrophy and contractile dysfunction. The present study aimed to delineate metabolic cardiomyopathies underlying the etiology of obesity-associated cardiac pathology. Metabolic measurements were made in hens continued on R rations or assigned to AL feeding after 7 d and 21 days. AL feeding increased plasma insulin, glucose, and non-esterified fatty acid (NEFA) concentrations by 21 d (P < 0.05). Metabolic cardiomyopathy in AL-hens was confirmed by cardiac triacylglycerol (TG) and ceramide accumulation consistent with up-regulation of related enzyme gene expressions, and by increased indices of oxidation stress (P < 0.05). In contrast to R hens, cardiac pyruvate dehydrogenase (PDH) activity and glucose transporter (GLUT) gene expressions increased progressively while carnitine palmitoyltransferase-1 (CPT-1) transcript levels in AL hens declined from 7 d to 21 d (P < 0.05), reflecting a shift from an oxidative to a more glycolytic metabolism, a typical metabolic derangement associated with cardiac hypertrophic remodeling. Cardiac pathogenesis in AL hens was further indicated by increased leukocyte infiltrates, interleukin-1β (IL-1β) and IL-6 production, cellular apoptosis, interstitial fibrosis, and expression of the heart failure marker myosin heavy chain (MHC-β; cardiac muscle beta) (P < 0.05). Results support the conclusion that diabetic conditions, cardiac inflammation and lipotoxic metabolic derangements act as pathological cues to trigger pathogenic changes along cardiac hypertrophy in AL hens.
采食量通常受到限制（R）以避免肥胖并提高产蛋量和成活率。为了确定改善心脏健康是否有助于提高成活率，完全成年的 45 周龄 R 母鸡被允许自由采食（AL）长达 10 周（70 天）。在 70 天时，对死亡率、收缩功能和形态进行了测量，并在 R 和 AL 母鸡之间进行了比较。分别报告了心脏电生理学和死亡率的结果，发现 AL 母鸡的死亡率增加与心脏病理性肥大和收缩功能障碍有关。本研究旨在描绘肥胖相关心脏病理学病因学中的代谢性心肌病。在 7 天和 21 天后，继续给予 R 日粮的母鸡或分配给 AL 喂养的母鸡进行代谢测量。AL 喂养在 21 天时增加了血浆胰岛素、葡萄糖和非酯化脂肪酸（NEFA）浓度（P < 0.05）。AL-母鸡的代谢性心肌病通过心脏三酰甘油（TG）和神经酰胺的积累得到证实，这与相关酶基因表达的上调一致，并通过氧化应激指数的增加得到证实（P < 0.05）。与 R 母鸡不同，心脏丙酮酸脱氢酶（PDH）活性和葡萄糖转运体（GLUT）基因表达逐渐增加，而 AL 母鸡的肉碱棕榈酰转移酶-1（CPT-1）转录水平从 7 天到 21 天下降（P < 0.05），反映了从氧化代谢向更糖酵解代谢的转变，这是与心脏肥大重塑相关的典型代谢紊乱。AL 母鸡的心脏发病机制还表现在白细胞浸润增加、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）产生增加、细胞凋亡、间质纤维化和心力衰竭标志物肌球蛋白重链（MHC-β；心肌β）表达增加（P < 0.05）。结果支持这样的结论，即糖尿病状态、心脏炎症和脂肪毒性代谢紊乱作为病理性线索，触发 AL 母鸡心脏肥大过程中的病理变化。
