Obesity-associated cardiac pathogenesis in broiler breeder hens: Pathological adaption of cardiac hypertrophy1,2

被引:16
作者
Chen, C. Y. [1 ]
Lin, H. Y. [1 ]
Chen, Y. W. [1 ]
Ko, Y. J. [1 ]
Liu, Y. J. [1 ]
Chen, Y. H. [1 ]
Walzem, R. L. [2 ]
Chen, S. E. [1 ,3 ,4 ]
机构
[1] Natl Chung Hsing Univ, Dept Anim Sci, Taichung, Taiwan
[2] Texas A&M Univ, Dept Poultry Sci, College Stn, TX USA
[3] Natl Chung Hsing Univ, Agr Biotechnol Ctr, Taichung, Taiwan
[4] Natl Chung Hsing Univ, iEGG Ctr, Ctr Integrat & Evolutionary Galliformes Genom, Taichung, Taiwan
关键词
broiler breeder hens; cardiac hypertrophy; ventricle dilation; arrhythmia; mortality; REPRODUCTIVE-PERFORMANCE; FEED RESTRICTION; ASCITES SYNDROME; HEART-FAILURE; CHICKENS; ACID; LIPOTOXICITY; DYSFUNCTION; GROWTH;
D O I
10.3382/ps/pex015
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
Broiler hens consuming feed to appetite (ad libitum; AL) show increased mortality. Feed restriction (R) typically improves reproductive performance and livability of hens. Rapidly growing broilers can exhibit increased mortality due to cardiac insufficiency but it is unknown whether the increased mortality of non-R broiler hens is also due to cardiac compromise. To assess cardiac growth and physiology in fully mature birds, 45-week-old hens were either continued on R rations or assigned to AL feeding for 7 or 21 days. AL hens exhibited increased bodyweight, adiposity, absolute and relative heart weight, ventricular hypertrophy, and cardiac protein/ DNA ratio by d 21 (P < 0.05). Increased heart weights due to hypertrophic growth was attributed to enhanced IGF-1-Akt-FoxO1 signaling and its downstream target, translation initiation factor 4E-BP1 in conjunction with down-regulation of ubiquitin ligase atrogin-1/MAFbx (P < 0.05). Reduced activation of cardiac AMPK and downstream activation of ACC-1 in parallel with increased cardiac nitric oxide levels, calcineurin activity, and MAPK activation in AL hens (P < 0.05) suggested that metabolic derangement develops along the cardiovascular remodeling. These indictors of cardiac maladaptive hypertrophic growth were further supported by uregulation of heart failure markers, BNP and MHC-beta (P < 0.05). Hens allowed AL feeding for 70 d exhibited a higher incidence of mortality (40% vs. 10%) in association with ascites, pericardial effusion, and ventricle dilation. A higher incidence of irregular ECG patterns and rhythmicity consistent with persistently elevated systolic blood pressure and ventricle fibrosis were observed in AL hens (P < 0.05). These observations support the conclusion that AL feeding in broiler hens results in maladaptive cardiac hypertrophy that progresses to overt pathogenesis in contractility and thereby increases mortality. Feed restriction provides clear physiological benefit to heart function of adult broiler hens.
引用
收藏
页码:2428 / 2437
页数:10
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