分子营养

叶酸对超早期断奶宫内发育迟缓仔猪肝脏结构和细胞凋亡相关基因表达的影响

展开
  • 四川农业大学动物营养研究所,动物抗病营养四川省重点实验室,雅安 625014
姚 英(1987—),女,四川巴中人,硕士研究生,从事动物营养和饲料科学的研究。E-mail: ayaoying2005@163.com

收稿日期: 2011-08-11

  网络出版日期: 2012-02-07

基金资助

教育部创新团队猪抗病营养分子机制研究项目(IRTO555-5)

Folic Acid in Intrauterine Growth Retarded Early Weaner Piglets: Effects on Hepatic Structure and Apoptosis-Related Gene Expression

Expand
  • Key Laboratory of Sichuan Province, Animal Disease-Resistance Nutrition Institute of Animal Nutrition, Sichuan Agricultural University, Ya’an 625014, China

Received date: 2011-08-11

  Online published: 2012-02-07

摘要

本试验旨在研究饲粮添加不同水平叶酸对超早期断奶宫内发育迟缓(IUGR)仔猪肝脏结构和细胞凋亡相关基因表达的影响。选取24头14日龄断奶、平均体重(2.79±0.34) kg的"杜×长×大"三元杂交仔公猪,随机分为3个处理,分别饲喂在基础饲粮中添加0、5和10 mg/kg叶酸的试验饲粮,每个处理8个重复,每个重复1头猪。试验期21 d。结果表明:1)饲粮添加叶酸对35日龄仔猪血清葡萄糖浓度无显著影响(P>0.05),添加5和10 mg/kg叶酸分别显著(P<0.05)和极显著(P<0.01)降低了血清甘油三酯浓度。2)饲粮添加5 mg/kg叶酸能显著降低肝细胞直径(P<0.05)。3)饲粮添加5 mg/kg叶酸显著提高了肝脏B细胞淋巴瘤蛋白2(Bcl-2)的基因表达量(P<0.05),极显著降低了Bcl-2相关X蛋白(Bax)和促凋亡相关基因肿瘤蛋白53(p53)的基因表达量(P<0.01);饲粮添加10 mg/kg叶酸,Bax和p53的基因表达量分别极显著(P<0.01)和显著(P<0.05)地降低了。4)饲粮添加叶酸对肝脏毛细血管扩张性共济失调症突变基因(ATM)、脱嘌呤嘧啶核酸内切酶1(APE-1)基因和一碳单位代谢关键酶编码基因的表达无显著影响(P>0.05)。结果提示,饲粮补充一定水平的叶酸有助于改善早期断奶IUGR仔猪35日龄时肝脏结构和细胞凋亡相关基因Bcl-2、Baxp53的表达;本试验条件下,饲粮添加5 mg/kg叶酸效果较好。

本文引用格式

姚英, 陈代文, 刘静波, 毛湘冰, 毛倩, 余冰 . 叶酸对超早期断奶宫内发育迟缓仔猪肝脏结构和细胞凋亡相关基因表达的影响[J]. 动物营养学报, 2012 , 24(2) : 271 -279 . DOI: 10.3969/j.issn.1006-267x.2012.02.012

Abstract

This experiment was conducted to study the effects of dietary folic acid level on hepatic structure and apoptosis-related gene expression in early weaner piglets suffered intrauterine growth retardation (IUGR). Twenty four crossbred (Duroc×Landrace×Yorkshire) male piglets, weaned at 14 days of age, with an average body weight of (2.79±0.34) kg were randomly assigned into 3 groups with 8 replicates in each group and 1 piglet per replicate. Piglets were fed diets supplemented with 0, 5 and 10 mg/kg folic acid, respectively. The experiment lasted for 21 d. The results showed as follows: 1) dietary supplementation of 5 (P<0.05) and 10 mg/kg (P<0.01) folic acid significantly decreased serum triglycerides concentration of piglets at 35 days of age, but had no significant effect on serum glucose concentration (P>0.05). 2) Dietary supplementation of 5 mg/kg folic acid significantly decreased hepatocyte diameter (P<0.05). 3) Dietary supplementation of 5 mg/kg folic acid significantly up-regulated gene expression of Bcl-2 (P<0.05), but significantly down-regulated gene expression of Bax and p53 (P<0.01); however, gene expression of Bax (P<0.01) and p53 (P<0.05) was significantly reduced by dietary supplementation of 10 mg/kg folic acid. 4) Expression of ATM and APE-1 as well as key enzyme encoding genes involved in one-carbon metabolism was not affected by folic acid supplementation. These results indicate that supplementation of folic acid at proper level can improve hepatic structure and apoptosis-related gene (Bcl-2, Bax and p53) expression of IUGR piglets; under conditions in this experiment, the optimum level is 5 mg/kg.

参考文献

[1] DESAI M, CROWTHER N J, LUCAS A, et al. Organ-selective growth in the offspring of protein-restricted mothers[J]. British Journal of Nutrition, 1996, 76(4):591-603.  



[2] MORTENSEN O H, OLSEN H L, FRANDSEN L, et al. Gestational protein restriction in mice has pronounced effects on gene expression in newborn offspring’s liver and skeletal muscle: protective effect of taurine[J]. Pediatric Research, 2009, 67(1):47-53.



[3] BUFFAT C, BOUBRED F, MONDON F, et al. Kidney gene expression analysis in a rat model of intrauterine growth restriction reveals massive alterations of coagulation genes[J]. Endocrinology, 2007, 148(11):5549-5557.  



[4] 刘静波,姚英,余冰,等.叶酸对初产母猪繁殖性能和宫内发育迟缓仔猪肾脏功能基因表达的影响[J].动物营养学报,2010,22(2):278-284.



[5] BURDGE G C, LILLYCROP K A, PHILLIPS E S, et al. Folic acid supplementation during the juvenile-pubertal period in rats modifies the phenotype and epigenotype induced by prenatal nutrition[J]. The Journal of Nutrition, 2009, 139(6):1054-1060.  



[6] BASERGA M, HALE M A, MCKNIGHT R A, et al. Uteroplacental insufficiency alters hepatic expression, phosphorylation, and activity of the glucocorticoid receptor in fetal IUGR rats[J]. The American Journal of Physiology, 2005, 289(5):1348-1353.



[7] CORTEZ D, WANG Y, QIN J, et al. Requirement of ATM-dependent phosphorylation of brca1 in the DNA damage response to double-strand breaks[J]. Science, 1999, 286:1162-1166.



[8] 汤显斌,谭云山.脱嘌呤嘧啶核酸内切酶与肿瘤相关性研究进展[J].国外医学:肿瘤学分册,2003,30:249-251.



[9] BAILEY L B, GREGORY J F. Folate metabolism and requirements[J]. The Journal of Nutrition, 1999, 129(4):779-782.



[10] HUANG R F S, HO Y H, LIN H L, et al. Folate deficiency induces a cell cycle-specific apoptosis in HepG2 cells[J]. The Journal of Nutrition, 1999, 129(1):25-31.



[11] RONCALES M, ACHON M, MANZARBEITIA F, et al. Folic acid supplementation for 4 weeks affects liver morphology in aged rats[J]. The Journal of Nutrition, 2004, 134(5):1130-1133.



[12] KOTSOPOULOS J, SOHN K J, KIM Y I. Postweaning dietary folate deficiency provided through childhood to puberty permanently increases genomic DNA methylation in adult rat liver[J]. The Journal of Nutrition, 2008, 138(4):703-709.



[13] GODFREY K M, GLUCKMAN P D, HANSON M A. Developmental origins of metabolic disease: life course and intergenerational perspectives[J]. Trends in Endocrinology & Metabolism, 2010, 21(4):199-205.  



[14] PFAFFL M W. A new mathematical model for relative quantification in real-time RT-PCR[J]. Nucleic Acids Research, 2001, 29(9):e45.



[15] 孔祥峰,吴国耀,印遇龙.猪宫内发育迟缓及其防治研究进展[J].畜牧与兽医,2009(10):96-101.



[16] PINNEY S E, SIMMONS R A. Epigenetic mechanisms in the development of type 2 diabetes[J]. Trends in Endocrinology and Metabolism, 2009, 21(4):223-229.



[17] WHITTEMORE C T, TULLIS J B, EMMANS G C. Protein growth in pigs[J]. Animal Production, 1988, 46(3):437-445.  



[18] BURDGE G C, LILLYCROP K A, JACKSON A A, et al. The nature of the growth pattern and of the metabolic response to fasting in the rat are dependent upon the dietary protein and folic acid intakes of their pregnant dams and post-weaning fat consumption[J]. British Journal of Nutrition, 2008, 99(3):540-549.



[19] KORSMEYER S J, SHUTTER J R, VEIS D J, et al. Bcl-2/Bax: a rheostat that regulates an anti-oxidant pathway and cell death[J]. Seminars in Cancer Biology, 1993, 4(6):327-332.



[20] PHAM T D, MACLENNAN N K, CHIU C T, et al. Uteroplacental insufficiency increases apoptosis and alters p53 gene methylation in the full-term IUGR rat kidney[J]. American Journal of Physiology, 2003, 285(5):962-970.



[21] BAGNYUKOVA T V, POWELL C L, PAVLIV O, et al. Induction of oxidative stress and DNA damage in rat brain by a folate/methyl-deficient diet[J]. Brain Research, 2008, 1237:44-51.



[22] LIU J, CHEN D, MAO X, et al. Effects of maternal folic acid supplementation on morphology and apoptosis-related gene expression in jejunum of newborn intrauterine growth retarded piglets[J]. Archives of Animal Nutrition, 2011, 65(5):376-385.  



[23] ACHON M, REYES L, ALONSO-APERTE E, et al. High dietary folate supplementation affects gestational development and dietary protein utilization in rats[J]. The Journal of Nutrition, 1999, 129(6):1204-1208.



[24] CARNEY E, CANADA T. Dietary folate and vitamin B12 intake and cognitive decline among community-dwelling older persons[J]. Nutrition in Clinical Practice, 2006, 21(2):188-189.  



[25] ULRICH C M, POTTER J D. Folate supplementation: too much of a good thing? [J] Cancer Epidemiology Biomarkers & Prevention, 2006, 15(2):189-193.



[26] ENGEHAM S F, HAASE A, LANGLEY-EVANS S C. Supplementation of a maternal low-protein diet in rat pregnancy with folic acid ameliorates programming effects upon feeding behaviour in the absence of disturbances to the methionine-homocysteine cycle[J]. British Journal of Nutrition, 2010, 103(7):996-1007.  



[27] REED M C, NIJHOUT H F, NEUHOUSER M L, et al. A mathematical model gives insights into nutritional and genetic aspects of folate-mediated one-carbon metabolism[J]. The Journal of Nutrition, 2006, 136(10):2653-2661.



[28] NIJHOUT H F, REED M C, BUDU P, et al. A mathematical model of the folate Cycle[J]. Journal of Biological Chemistry, 2004, 279(53):55008-55016.  



[29] ULRICH C M, REED M C, NIJHOUT H F. Modeling folate, one-carbon metabolism, and DNA methylation[J]. Nutrition Reviews, 2008, 66:27-30.
文章导航

/