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

LIU Lei, SONG Zhigang, KONG Xue, JIAO Hongchao, LIN Hai

doi:10.3969/j.issn.1006-267x.2012.01.014

2012 , Vol. 24 >Issue 1: 95 - 103

DOI: https://doi.org/10.3969/j.issn.1006-267x.2012.01.014

Molecular Nutrition

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

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

Received date: 2011-08-31

Online published: 2012-01-13

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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.

Key words： dexamethasone; dietary energy level; feed intake; neuropeptide Y; broiler chickens

Cite this article

LIU Lei, SONG Zhigang, KONG Xue, JIAO Hongchao, LIN Hai . Effects of Dexamethasone and Dietary Energy Level on Energy Intake and Neuropeptide Y Gene Expression of Broiler Chickens[J]. Chinese Journal of Animal Nutrition, 2012 , 24(1) : 95 -103 . DOI: 10.3969/j.issn.1006-267x.2012.01.014

References

[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.

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