Dietary Supplementation of 25-Hydroxycholecalciferol Improves Livability in Broiler Breeder Hens-Amelioration of Cardiac Pathogenesis and Hepatopathology
Dietary Supplementation of 25-Hydroxycholecalciferol Improves Livability in Broiler Breeder Hens-Amelioration of Cardiac Pathogenesis and Hepatopathology
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DOI：
10.3390/ani9100770
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发表时间：
2019-10-01
期刊：
影响因子：
3
通讯作者：
Chen, Shuen-Ei
中科院分区：
文献类型：
--
作者：
Lin, Hsuan-Yu;Chou, Pao-Chia;Chen, Shuen-Ei
具有较高体重（BW）和脂肪积累的肉种鸡较早地遭受猝死，同时伴有心律失常和过度通气。病理性心脏肥大和功能衰竭是肝脏病理学加重猝死的原因。日粮中添加25-OH-D3通过改善系统性缺氧、酸中毒、以及通过钙调神经磷酸酶-NFAT 4c信号传导和MHC-β表达与减少肝脏脂肪变性和纤维化相关的心脏病理性肥大。摘要补充69微克25-羟基胆钙化醇在26-60周龄的饲养试验中，（25-OH-D3）/kg饲料使饲料限制（R-母鸡）肉种鸡的存活率增加9.9%，使允许自由采食饲料的母鸡（Ad-母鸡）的存活率增加65.6%。体重较高和/或肥胖的母鸡较早发生猝死（SD），并伴有心律失常和过度通气。在对同一群母鸡的研究中，我们证明25-OH-D3通过改善全身性缺氧、酸中毒和心脏病理性肥大（经由钙调神经磷酸酶-NFAT 4c信号传导和MHC-β表达，与降低的血浆三酰甘油和肝脂肪变性和纤维化相关）来改善母鸡的存活率和心脏健康（p < 0.05）。与在29、35和47周取样的活母鸡相反，SD母鸡表现出严重的心脏肥大，其为进行性的（Ad组）或稳定的（R组）。随着研究的进行，任何组SD母鸡的实际和相对肝脏重量均下降。心脏重量显着相关的总重量和相对肝脏重量在SD母鸡的R-和AD-组。与在35和47周取样的正常对照相比，表现出心脏肥大的R-母鸡经历了严重的缺氧和酸中毒，体重、肝脏和心脏的绝对和相对重量、肝脏和血浆三酰甘油含量增加，以及心律失常（p < 0.05）。目前的研究结果表明，病理性心脏肥大和功能衰竭是SD的致病因素，这种致病性的进展是加速肝脏病理学，特别是在早期的年龄。饲料效率的提高伴随着体重和脂肪的快速增加，增加了母鸡缺氧、不可逆心脏肥大和心律失常的风险，这些风险导致功能受损和SD。在基础日粮中添加69 mg/kg饲料的25-OH-D3可有效改善肉种母鸡的心脏发病机制并预防SD。
Simple Summary Broiler breeder hens with higher bodyweights (BW) and fat accumulation suffered sudden death earlier in conjunction with compromised heart rhythms and over-ventilation. Pathological cardiac hypertrophy and functional failure are causative factors of sudden death with exacerbation by hepatopathology. Dietary 25-OH-D3 supplementation improved hen's livability and heart health by ameliorating systemic hypoxia, acidosis, and cardiac pathological hypertrophy through calcineurin-NFAT4c signaling and MHC-beta expression in association with reduced hepatic steatosis and fibrosis.Abstract A supplement of 69 mu g 25-hydroxycholecalciferol (25-OH-D3)/kg feed increased livability in feed restricted (R-hens) broiler breeder hens by 9.9% and by 65.6% in hens allowed ad libitum feed intake (Ad-hens) in a feeding trial from age 26-60 weeks. Hens with higher bodyweight and/or adiposity suffered sudden death (SD) earlier in conjunction with compromised heart rhythms and over-ventilation. In the study with the same flock of hens, we demonstrate that 25-OH-D3 improved hen's livability and heart health by ameliorating systemic hypoxia, acidosis, and cardiac pathological hypertrophy through calcineurin-NFAT4c signaling and MHC-beta expression in association with reduced plasma triacylglycerol and hepatic steatosis and fibrosis (p < 0.05). In contrast to live hens sampled at 29, 35, and 47 weeks, SD hens exhibited severe cardiac hypertrophy that was either progressive (Ad-groups) or stable (R-groups). Actual and relative liver weights in SD hens from any group declined as the study progressed. Heart weight correlated significantly to total and relative liver weights in SD-hens of both R- and Ad-groups. In contrast to normal counterparts sampled at 35 and 47 weeks, R-hens exhibiting cardiac hypertrophy experienced severe hypoxia and acidosis, with increased bodyweight, absolute and relative weights of liver and heart, hepatic and plasma triacylglycerol content, and cardiac arrhythmia (p < 0.05). The present results demonstrate that pathological cardiac hypertrophy and functional failure are causative factors of SD and this pathogenic progression is accelerated by hepatopathology, particularly during the early age. Increased feed efficiency with rapid gains in BW and fat increase hens' risk for hypoxia, irreversible cardiac hypertrophy, and arrhythmias that cause functional compromise and SD. Additional supplementation of 69 mg/kg feed of 25-OH-D3 to the basal diet is effective to ameliorate cardiac pathogenesis and prevent SD in broiler breeder hens.