分子营养

地塞米松和饲粮能量水平对肉仔鸡能量采食及神经肽Y基因表达的影响

展开
  • 山东农业大学动物科技学院, 泰安 271018
刘 磊(1985—),男,山东青州人,博士研究生,从事家禽生态营养研究。E-mail: liusanshi1985@126.com

收稿日期: 2011-08-31

  网络出版日期: 2012-01-13

基金资助

国家自然科学基金(31072045);公益性行业(农业)科研专项(201003011)

Effects of Dexamethasone and Dietary Energy Level on Energy Intake and Neuropeptide Y Gene Expression of Broiler Chickens

Expand
  • College of Animal Science and Technology, Shandong Agricultural University, Tai'an 271018, China

Received date: 2011-08-31

  Online published: 2012-01-13

摘要

本试验旨在探讨注射地塞米松(DEX)模拟应激状态下,应激和饲粮能量水平对肉仔鸡能量采食的影响。选取体重相近的180只23日龄的雄性爱拔益加(AA)肉鸡随机分成6组,每组3个重复,每个重复10只鸡。试验采用2×3析因设计,因素为DEX[处理(注射DEX2 mg/kg)、未处理(注射等剂量生理盐水)]和饲粮能量水平[高能(HE)、低能(LE)以及高能、低能自由采食(H-LE)]。预试期5 d,正试期7 d。结果表明:1)DEX处理极显著降低了肉仔鸡的采食量和体增重(P<0.01),极显著提高了耗料增重比、耗能增重比、腹脂率以及血浆葡萄糖、甘油三酯和尿酸的浓度(P<0.01),显著提高了肠道指数(P<0.05)。2)采用LE饲粮体增重(P<0.05)、腹脂率(P<0.01)显著低于其他2种饲粮,耗料增重比显著低于HE饲粮(P<0.05);采用HE饲粮耗能增重比极显著高于其他2种饲粮(P<0.01);采用H-LE饲粮神经肽Y(NPY)基因表达量显著高于LE饲粮(P<0.05)。3)DEX、饲粮能量水平对耗料增重比(P<0.05)和耗能增重比(P<0.01)的影响存在显著的互作效应。结果提示,DEX应激可使肉仔鸡血浆中葡萄糖、尿酸和甘油三酯的浓度升高;DEX应激和HE饲粮均能增加脂肪在腹部沉积,提高耗料增重比和耗能增重比;H-LE饲粮能上调肉仔鸡下丘脑NPY基因表达。

本文引用格式

刘磊, 宋志刚, 孔雪, 焦洪超, 林海 . 地塞米松和饲粮能量水平对肉仔鸡能量采食及神经肽Y基因表达的影响[J]. 动物营养学报, 2012 , 24(1) : 95 -103 . DOI: 10.3969/j.issn.1006-267x.2012.01.014

Abstract

This experiment was conducted to investigate effects of dexamethasone (DEX) and dietary energy level on the energy intake of broiler chickens under the simulative stress induced by DEX injection. One hundred and eighty 23-day-old male broiler chickens (Arbor Acres) were selected and randomly divided into 6 groups with 3 replicates in each group and 10 chickens per replicate. A 2×3 factorial design was used. The factors were DEX [treated(injected with 2 mg/kg DEX) and untreated (injected with physiological saline at an equal dose)] and dietary energy level [high energy(HE), low energy (LE) and freely choose between HE and LE(H-LE)]. The pre-experiment lasted for 5 d, and the experiment lasted for 7 d. The results showed as follows: 1) DEX treatment significantly decreased feed intake (P<0.01) and body weight gain (P<0.01), but significantly increased feed/gain (P<0.01), energy/gain (P<0.01), abdominal fat percentage (P<0.01), plasma concentrations of glucose, triglyceride and urate (P<0.01), as well as intestinal tract index (P<0.05). 2) Broiler chickens fed LE diet had significantly lower body weight (P<0.05) and abdominal fat percentage (P<0.01) than those fed the other two kinds of diets, and had significantly lower feed/gain than those fed HE diet (P<0.01); broiler chickens fed HE diet had significantly higher energy/gain than those fed the other two kinds of diets (P<0.01); broiler chickens fed H-LE diet had significantly higher gene expression level of NPY than those fed LE diet (P<0.05). 3) DEX and dietary energy level had significant interaction effects on feed/gain (P<0.05) and energy/gain (P<0.01). The results indicate that DEX-stress can increase plasma concentrations of glucose, triglyceride and urate; both DEX-stress and HE diet can increase deposition of abdominal fat, feed/gain and energy/gain; H-LE diet can increase NPY gene expression in the hypothalamus of broiler chickens.

参考文献

[1] 孔雪.糖皮质激素调控家禽采食的机制[D].硕士学位论文.泰安:山东农业大学,2010:35-47.

[2] 袁磊.应激对肉鸡采食量影响及其调节机制[D].硕士学位论文.泰安:山东农业大学,2007:31-45.

[3] 姜克杰.应激和饲粮能量水平对肉鸡生长发育和脂肪代谢的影响[D].硕士学位论文.泰安:山东农业大学,2007:15-16.

[4] ZULKIFLIA I, SIEGE P B. Is there a positive side to stress?[J]. World's Poultry Science Journal, 1995, 51(1):63-76.  

[5] FOUCAUD L, NIOT I, KANDA T, et al. Indirect dexamethasone down-regulation of the liver fatty acid-binding protein expression in rat liver[J]. Biochimica et Biophysica Acta, 1998, 1391(2):204-212.

[6] QI D, PULINILKUNNIL T, AN D, et al. Single-dose dexamethasone induces whole-body insulin resistance and alters both cardiac fatty acid and carbohydrate metabolism[J]. Diabetes, 2004, 53(7):1790-1797.  

[7] CAI Y, SONG Z, WANG X, et al. Dexamethasone-induced hepatic lipogenesis is insulin dependent in chickens (Gallus gallus domesticus)[J]. Stress, 2011, 14(3):273-281.

[8] CAI Y, SONG Z, ZHANG X, et al. Increased de novo lipogenesis in liver contributes to the augmented fat deposition in dexamethasone exposed broiler chickens (Gallus gallus domesticus)[J]. Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology, 2009, 150(2):164-169.  

[9] WANG X, LIN H, SONG Z, et al. Dexamethasone facilitates lipid accumulation and mild feed restriction improves fatty acids oxidation in skeletal muscle of broiler chicks (Gallus gallus domesticus)[J]. Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology, 2010, 151(4):447-454.  

[10] TOMASZUK A, SIMPSON C, WILLIAMS G. Neuropeptide Y, the hypothalamus and the regulation of energy homeostasis[J]. Hormone Research in Paediatrics, 1996, 46(2):53-58.

[11] KALRA S P, HORVATH T L. Neuroendocrine interactions between galanin, opioids, and neuropeptide Y in the control of reproduction and appetite[J]. Annals of the New York Academy of Sciences, 1998, 863(1):236-240.  

[12] KOVACS K J, WESTPHAL H M, PECZELY P. Distribution of glucocorticoid receptor-like immunoreactivity in the brain, and its relation to CRF and ACTH immunoreactivity in the hypothalamus of the Japanese quail, coturnix coturnix japonica[J]. Brain Research, 1989, 505(2):239-245.  

[13] LIVAK K J, SEHMITTGEN T D. Analysis of relative gene expression data using rea1-time quantitative PCR and the 2‐ΔΔCt method[J]. Methods, 2001, 25(4):402-408.  

[14] HERMIER D. Lipoprotein metabolism and fattening in poultry[J]. The Journal of Nutrition, 1997, 127(5):805S-808S.

[15] LIN H, DECUYPERE E, BUYSE J. Oxidative stress induced by corticosterone administration in broiler chickens (Gallus gallus domesticus): 1. Chronic exposure[J]. Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology, 2004, 139(4):737-744.  

[16] KITRAKI E, SOULIS G, GEROZISSIS K. Impaired neuroendocrine response to stress following a short-term fat-enriched diet[J]. Neuroendocrinology, 2004, 79(6):338-345.  

[17] MENCONI M, GONNELLA P, PETKOVA V, et al. Dexamethasone and corticosterone induce similar, but not identical, muscle wasting responses in cultured L6 and C2C12 myotubes[J]. Journal of Cellular Biochemistry, 2008, 105(2):353-364.  

[18] MALHEIROS R D, MORAES V M, COLLIN A, et al. Free diet selection by broilers as influenced by dietary macronutrient ratio and corticosterone supplementation. 1. Diet selection, organ weights, and plasma metabolites[J]. Poultry Science, 2003, 82(1):123-131.

[19] BARTOV I, JENSEN L S, VELTMANN, Jr. Effect of dietary protein and fat levels on fattening of corticosterone-injected broiler chicks[J]. Poultry Science, 1980, 59(8):1864-1872.

[20] HAYASHI K, KAYALI A G, TOMITA Y. Reduction of corticosterone-induced growth impairment by testosterone and its mechanism[J]. Journal of Animal Science and Technology, 1992, 63(10):1001-1008.

[21] REBUFFE-SCRIVA M, WALSH U A, MCEWEN B, et al. Effect of chronic stress and exogenous glucocorticoids on regional fat distribution and metabolism[J]. Physiology & Behavior, 1992, 52(3):583-590.  

[22] LIN H, SUI S J, JIAO H C, et al. Impaired development of broiler chickens by stress mimicked by corticosterone exposure[J]. Comparative Biochemistry and Physiology-Part A: Molecular & Integrative Physiology, 2006, 143(3):400-405.  

[23] ELWINGER K. Performance and abdominal and carcass fat in broilers as influenced by strain and diet energy concentration[C]//Proceedings 6th European Poultry Conference. Hamburg:[s.n.], 1980:256-263.

[24] MANTHA L, PALACIOS E, DESHAIES Y. Modulation of triglyceride metabolism by glucocorticoids in diet-induced obesity[J]. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, 1999, 277(2):R455-R464.

[25] COVASAA M, FORBESA J M. Selection of foods by broiler chickens following corticosterone administration[J]. British Poultry Science, 1995, 36(3):489-501.  

[26] BLIGH M E, DOUGLASS L W, CASTONGUAY T W. Corticosterone modulation of dietary selection patterns[J]. Physiology & Behavior, 1993, 53(5):975-982.  

[27] DENBOW D M. Food intake control in birds[J]. Neuroscience & Biobehavioral Reviews, 1985, 9(2):223-232.  

[28] MAYER J, THOMAS D W. Regulation of food intake and obesity[J]. Science, 1967, 156:328-337.

[29] EDWARDS C M, ABBOTT C R, SUNTER D, et al. Cocaine-and amphetamine-regulated transcript, glucagon-like peptide-1 and corticotrophin releasing factor inhibit feeding via agouti-related protein independent pathways in the rat[J]. Brain Research, 2000, 866(1/2):128-134.

[30] ZAKRZEWSKA J M, CHAUDHRY Z, NURMIKKO T J, et al. Lamotrigine (lamictal) in refractory trigeminal neuralgia: results from a double-blind placebo controlled crossover trial[J]. Pain, 1997, 73(2):223-230.  

[31] MATTERI R L. Overview of central targets for appetite regulation[J]. Journal of Animal Science, 2001, 79(E-Suppl.):E148-E158.

[32] SHIMIZU H, ARIMA H, OZAWA Y, et al. Glucocorticoids increase NPY gene expression in the arcuate nucleus by inhibiting mTOR signaling in rat hypothalamic organotypic cultures[J]. Peptides, 2010, 31(1):145-149.  

[33] MEIJER O C, DE LANGE E C, BREIMER D D, et al. Penetration of dexamethasone into brain glucocorticoid targets is enhanced in mdr1A P-glycoprotein knockout mice[J]. Endocrinology, 1998, 139(4):1789-1793.  

[34] GIRAUDO S Q, KOTZ C M, GRACE M K, et al. Rat hypothalamic NPY mRNA and brown fat uncoupling protein mRNA after high-carbohydrate or high-fat diets[J]. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, 1994, 266:R1578-R1583.

[35] LIN S, STORLIEN L H, HUANG X F. Leptin receptor, NPY, POMC mRNA expression in the diet-induced obese mouse brain[J]. Brain Research, 2000, 875:89-95.
文章导航

/