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標題: 肉用與蛋用母雞於不同能量狀態下其下視丘基因之表現及飼糧中甘胺酸添加對白羅曼鵝生長與相關生理之影響
Hypothalamic gene expressions of meat- and egg- type hens under different energy statuses and effects of dietary glycine supplementation on growth performance and related physiology of Roman geese
作者: 林嘉雋
Lin, Chia-Chun
關鍵字: 甘胺酸;glycine;晝夜節律基因;下視丘;食慾調節;能量狀態;白羅曼鵝;肉用與蛋用雞;circadian genes;hypothalamus;appetite regulation;energy status;egg- and meat-type chickens;Roman geese
出版社: 動物科學系所
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現代雞的家畜化發生約在8000年前,而在100多年前家雞進一步歧化出肉用和蛋用的雞種,進而形成現今生殖與生長表型迥異的白肉雞與蛋雞。為探討家畜化過程中,肉用與蛋用雞種其如何達成現今此迥然不同表型,試驗一為使用約45週齡的白肉種雞 (Arbor Acres, AA) 與蛋雞 (ISA Brown),蛋雞分成兩種處理,一組限飼 (110g/d),另一組強迫灌食 (一天灌食143g的飼料),而白肉種雞分成限飼 (130g/d) 和任飼,餵飼21天。試驗一結果顯示,蛋雞灌食與白肉種雞任飼21天其體重、肝臟重、相對肝臟比率、腹脂重、相對腹脂比率和血糖,分別都顯著較蛋雞限飼組和白肉種雞限飼組來的高,而下視丘AMPK (AMP-activating protein kinase) 活性則相反,此顯示蛋雞灌食處理和白肉種雞任飼21天可能有傾向肥胖的趨勢。白肉種雞任飼組血液中正腎上腺素濃度顯著高於限飼組 ; 白肉種雞不論限飼或任飼血液中正腎上腺素濃度都顯著高於蛋雞灌食組和限飼組,此表示白肉種雞限飼和任飼組緊迫程度顯著較蛋雞灌食和限飼組來的高。於16:00起每6小時犧牲部份雞隻取下視丘檢測其晝夜節律與Gonadotropin-releasing hormone (GnRH) 相關基因表現之脈動,結果顯示,與限飼組相較下,蛋雞灌食組與種雞任飼組處在高能量狀態下,能量相關基因 (LKB1、SIRT1 and PGC-1α) 表達與脈動模式直接受到影響,並進一步直接或間接影響晝夜節律基因 (Bmal1、Clock、Cry、Per、E4bp4 and RORα) 與Egr-1和GnRH基因表達與脈動模式。此顯示高能狀態下會影響下視丘中能量相關基因、晝夜節律基因與Egr-1和GnRH基因正常的脈動,此可用來解釋雞家畜化時因食物供給充足,由半饑餓狀態轉變成長期體內能量飽和狀態,進而驅使其他基因途徑的歧異化,以致於造成生理與表型的差異諸如採食行為、活動能力、代謝活動、與緊迫調適。而後經長期選拔結果最後衍生出現今肉用與蛋用雞種。台灣屬於熱帶及亞熱帶地區,夏季高溫潮濕,導致鵝隻採食量降低影響肥育階段鵝隻生長,造成飼養業者經濟上的損失。研究指出,glycine在神經元中扮演興奮性神經傳導物質,經活化N-methyl-D-aspartate (NMDA) receptors,來促進食慾。為了促進夏季肥育期鵝隻,試驗二分別在八月和九月,使用8週齡的白羅曼鵝,公母各半,分成四種處理,在飼料中添加0%、1%、2%和4%甘胺酸 (glycine) 。試驗二結果顯示,飼料中添加2% glycine對採食量沒有太大的影響,但有提高的趨勢,而在淨增重與生長效率方面有較好的表現。添加高與低劑量的glycine對血液葡萄糖、三酸甘油脂、NEFA、與尿酸濃度皆無影響。飼料中添加1% glycine對肝臟、腿肌與會胸肌中三酸甘油脂含量有提高的趨勢。添加glycine整體而言會提高胸肌、腿肌、肝臟和脂肪組織脂肪合成基因 (acetyl-CoA carboxylase、fatty acid synthase、PPAR-γ and SREBP-1) 與胸肌肌肉合成基因 (IGF-1、growth hormone receptor、myostatin and leucyl-tRNA synthetase) 之表現,但添加高量的glycine則會降低其表現。添加glycine的處理組其促進食慾的NPY與抑制食慾BDNF和MC4R基因之表現都顯著下降,此表示,飼料中添加glycine會提高淨增重和飼料效率,但其對食慾調節相關基因沒有太大的影響。綜上所述,推薦夏季鵝隻飼料中添加2% glycine可促進鵝隻整體的生長表現,而glycine添加可能影響其他神經迴路最後導致對食慾調控基因沒有影響。

Along the history, chickens have been domesticated around 8000 years and populations bred for egg laying and meat production can be dated to about 100 years ago. During the twentieth century, growth performance (meat production) and reproductive efficacy (egg production) were further diverged to produce the modern layer and broiler strains. In order to explore the pathways that achieve the distinctively different phenotypes between egg-and meat-type chickens along domestication, in feeding trial 1 broiler breeder and ISA Brown layer hens were fed with restricted (130g/d) (BR) or ad libitum (BA) feeding and restricted (110g/d) (LR) or overfeeding (143g/d) (LO), respectively, for after 21 days to mimic domestication with sufficient fuel supply in contrast to their ancestors with semi-hunger status in the wild. Layers with overfeeding and broiler breeders with ad libitum feeding exhibited higher body weight, absolute and relative liver and abdominal fat weight and plasma glucose levels, but lower activation of AMPK (AMP-activated protein kinase) in the hypothalamus, suggesting obesity development in birds with higher energy status. A higher plasma norepinephrine levels was observed in BA birds than BR birds, but the difference was absent between LO and LR layers, suggesting that broiler breeders may keep adrenergic sensitivity in response to fuel stress. In contrast to birds with lower energy status (BR and LR), hypothalamic LKB1, SIRT1 and PGC-1α gene expression and pulsatile pattern were affected by higher energy status, leading to altered expression and pulsatile pattern of circadian genes in the hypothalamus including Bmal1, Clock, Cry, Per, E4bp4 and RORα and gonadotropin-releasing hormone (GnRH). These results thus may mimic the process that fuel saturation along domestication can drive the divergence of genetic pathways to achieve different phenotypes such as feeding behaviors, locomotor activities, metabolic regulations, stress adaptation that allow selection to proceed and thereby deviate to produce the modern chickens of egg- and meat-type strain. Taiwan is located in tropical and subtropical regions with high temperature and relative humidity under summer season. Finishing geese tend to have poor appetite during hot seasons in Taiwan, which impacts economical benefit. Glycine acts as a co-agonist of the N-methyl- D-aspartic acid (NMDA) receptors through excitatory neurotransmission to increase appetite. In order to increase feed intake of finishing geese during hot seasons in Taiwan, in feeding trial 2, geese at age of 8 weeks were fed diet supplemented with different levels of glycine (0%, 1%, 2% and 4% of feed) for 4 weeks during August and September. Results suggested that dietary supplementation of glycine, particularly at 2% level, significantly promoted daily feed efficiency and BW gain, but 2% level also significantly decreased fractional breast muscle weight. In plasma parameters, glycine inclusion exerted no significant effect on plasma glucose, non-esterified fatty acid (NEFA), triglyceride (TG) and uric acid level. Gene expressions relative to lipogenesis (acetyl-CoA carboxylase, fatty acid synthase, PPAR-γ and SREBP-1) in the leg muscle, breast muscle, liver, and adipose tissue and myogenic gene expressions (IGF-1, growth hormone receptor, myostatin, leucyl-tRNA synthetase) in the breast muscle were increased by dietary supplementation of lower glycine levels, but suppressed by the inclusion of a higher glycine level. Interestingly, hypothalamic neuropeptide Y (NPY), brain-derived neurotrophic factor (BDNF) and melanocortin 4 receptors (MC4R) expression was suppressed by dietary supplementation of glycine, suggest that glycine inclusion of feed decreased feed intake but had no effects on appetite gene expression. We concluded that dietary supplementation of glycine at 2% is the best recommendation use to promote geese growth performance during finishing period. Inconsistent results between NPY and BDNF expression suggest that other hypothalamic anorexigenic/orexigenic factors behind those examined in the current study are involved in regulating appetite by dietary glycine supplementation.
其他識別: U0005-0708201214221100
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