高低脂肉鸡中与腹脂沉积相关基因的差异表达
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摘要
试验以腹脂率(腹脂率=腹脂重/活重×100%)为标准选择两尾个体,分为高脂组(H)和低脂组(L),每组各6只,利用qRT-PCR的方法分析了与腹脂沉积相关的基因在鸡不同组织中的mRNA表达量。结果表明:LPIN1、ABHD5、ADORA1、ACBD5在肉鸡腹脂中高脂组的表达量低于低脂组,而DHCR24、SQLE在肉鸡腹脂中高脂组的表达量高于低脂组,且均差异显著,结果提示这些基因可能是影响肉鸡腹脂沉积的潜在分子标记。
Two-tailed individual birds were selected based on the ratio of abdominal fat content(abdominal fat rate=abdominal fat weight/live weight×100%), divided into high-fat group(H) and low-fat group(L)(6 birds in each group).The mRNA expression of genes associated with abdominal fat deposition in chicken different tissues was analyzed by qRT-PCR. The results showed that the expression levels of LPIN1, ABHD5, ADORA1, and ACBD5 in the abdominal fat of high-fat group were lower than those in the low-fat group, while the expression levels of DHCR24 and SQLE in the high-fat group of broiler abdominal fat were higher than those in the low-fat group. The results suggested that these genes may play a potential role in broiler abdominal fat deposition as molecular markers.
Two-tailed individual birds were selected based on the ratio of abdominal fat content(abdominal fat rate=abdominal fat weight/live weight×100%), divided into high-fat group(H) and low-fat group(L)(6 birds in each group).The mRNA expression of genes associated with abdominal fat deposition in chicken different tissues was analyzed by qRT-PCR. The results showed that the expression levels of LPIN1, ABHD5, ADORA1, and ACBD5 in the abdominal fat of high-fat group were lower than those in the low-fat group, while the expression levels of DHCR24 and SQLE in the high-fat group of broiler abdominal fat were higher than those in the low-fat group. The results suggested that these genes may play a potential role in broiler abdominal fat deposition as molecular markers.
引文
[1] HUANG H Y, LIU R R, ZHAO G P, et al.Integrated analysis of microRNA and mRNA expression profiles in abdominal adipose tissues in chickens[J]. Sci Rep, 2015,5:16132.
[2] RESNYK C W, CHEN C, HUANG H, et al.RNA-Seq Analysis of abdominal fat in genetically fat and lean chickens highlights a divergence in expression of genes controlling adiposity, hemostasis, and lipid metabolism[J]. PLoS One, 2015, 10(10):e139549.
[3] MUSRI M M, PARRIZAS M. Epigenetic regulation of adipogenesis[J]. Curr Opin Clin Nutr, 15(4):342-349.
[4] CHEN Y, RUI B, TANG L, et al. Lipin family proteinskey regulators in lipid metabolism[J]. Ann Nutr Metab,2015, 66(1):10-18.
[5] CORNACIU I, BOESZOERMENYI A, LINDERMUTH H, et al. The minimal domain of adipose triglyceride lipase(ATGL)ranges until leucine 254 and can be activated and inhibited by CGI-58 and G0S2, respectively[J]. PLoS One, 2011, 6(10):e26349.
[6] FAULHABER-WALTER R, JOU W, MIZEL D, et al. Impaired glucose tolerance in the absence of adenosine A1receptor signaling[J]. Diabetes, 2011, 60(10):2578-2587.
[7] JOHANSSON S M, SALEHI A, SANDSTROM M E, et al.A1 receptor deficiency causes increased insulin and glucagon secretion in mice[J]. Biochem Pharmacol, 2007, 74(11):1628-1635.
[8] NEESS D, BEK S, ENGELSBY H, et al. Long-chain acyl-CoA esters in metabolism and signaling:Role of acylCoA binding proteins[J]. Prog Lipid Res, 2015(59):1-25.
[9] TAKAHASHI T, GASCH A, NISHIZAWA N, et al. The DIMINUTO gene of Arabidopsis is involved in regulating cell elongation[J]. Genes and Development, 1995, 9(1):97-107.
[10] ZERENTURK E J, SHARPE L J, IKONEN E, et al. Desmosterol and DHCR24:Unexpected new directions for a terminal step in cholesterol synthesis[J]. Prog Lipid Res,2013, 52(4):666-680.
[11]周丽娜.SQLE调控ERK通路影响肺鳞癌细胞生长的机制[D].青岛:青岛大学, 2018.
[12] KERSHAW E E, FLIER J S. Adipose tissue as an endocrine organ[J]. J Clin Endocrinol Metab, 2004, 89(6):2548-2556.
[13]宋庆文.动物脂肪代谢过程中关键酶的研究进展[J].畜牧与饲料科学,2007(3):58-60.
[14] CHEN Y, RUI B B, TANG L Y, et al. Lipin family proteins-key regulators in lipid metabolism[J]. Ann Nutr Metab, 2015, 66(1):10-18.
[15] VAN HARMELEN V, RYDEN M, SJOLIN E, et al. A role of lipin in human obesity and insulin resistance:Relation to adipocyte glucose transport and GLUT4 expression[J]. J Lipid Res, 2007, 48(1):201-206.
[16] SERR J, SUH Y, LEE K. Cloning of comparative gene identification-58 gene in avian species and investigation of its developmental and nutritional regulation in chicken adipose tissue[J]. J Anim Sci, 2011, 89(11):3490-3500.
[17] FAULHABER-WALTER R, JOU W, MIZEL D, et al. Impaired glucose tolerance in the absence of adenosine A1receptor signaling[J]. Diabetes, 2011, 60(10):2578-2587.
[17] WATERHAM H R, KOSTER J, ROMEIJN G J, et al. Mutations in the 3beta-hydroxysterol Delta24-reductase gene cause desmosterolosis, an autosomal recessive disorder of cholesterol biosynthesis[J]. Am J Hum Genet, 2001, 69(4):685-694.
[18] HERZOG K, PRAS-RAVES M L, FERDINANDUSSE S,et al. Functional characterisation of peroxisomal beta-oxidation disorders in fibroblasts using lipidomics[J]. J Inherit Metab Dis, 2018, 41(3):479-487.
[19] YAGITA Y, SHINOHARA K, ABE Y, et al. Deficiency of a retinal dystrophy protein, Acyl-CoA binding domaincontaining 5(ACBD5), impairs peroxisomalβ-Oxidation of very-long-chain fatty acids[J]. J Biolo Chem, 2017,292(2):691-705.
[20] ZERENTURK E J, SHARPE L J, IKONEN E, et al. Desmosterol and DHCR24:Unexpected new directions for a terminal step in cholesterol synthesis[J]. Prog Lipid Res.2013, 52(4):666-680.
[21] ASTRUC M, TABACIK C, DESCOMPS B, et al. Squalene epoxidase and oxidosqualene lanosterol-cyclase activities in cholesterogenic and non-cholesterogenic tissues[J]. Biochim Biophys Acta, 1977, 487(1):204-211.
[22] SAWADA M, MATSUO M, HAGIHARA H, et al. Effect of FR194738, a potent inhibitor of squalene epoxidase,on cholesterol metabolism in HepG2 cells[J]. Eur J Pharmacol, 2001, 431(1):11-16.
[23] FERDINANDUSSE S, FALKENBERG K D, KOSTER J, et al. ACBD5 deficiency causes a defect in peroxisomal very long-chain fatty acid metabolism[J]. J Med Genet, 2017,54(5):330-337.
[2] RESNYK C W, CHEN C, HUANG H, et al.RNA-Seq Analysis of abdominal fat in genetically fat and lean chickens highlights a divergence in expression of genes controlling adiposity, hemostasis, and lipid metabolism[J]. PLoS One, 2015, 10(10):e139549.
[3] MUSRI M M, PARRIZAS M. Epigenetic regulation of adipogenesis[J]. Curr Opin Clin Nutr, 15(4):342-349.
[4] CHEN Y, RUI B, TANG L, et al. Lipin family proteinskey regulators in lipid metabolism[J]. Ann Nutr Metab,2015, 66(1):10-18.
[5] CORNACIU I, BOESZOERMENYI A, LINDERMUTH H, et al. The minimal domain of adipose triglyceride lipase(ATGL)ranges until leucine 254 and can be activated and inhibited by CGI-58 and G0S2, respectively[J]. PLoS One, 2011, 6(10):e26349.
[6] FAULHABER-WALTER R, JOU W, MIZEL D, et al. Impaired glucose tolerance in the absence of adenosine A1receptor signaling[J]. Diabetes, 2011, 60(10):2578-2587.
[7] JOHANSSON S M, SALEHI A, SANDSTROM M E, et al.A1 receptor deficiency causes increased insulin and glucagon secretion in mice[J]. Biochem Pharmacol, 2007, 74(11):1628-1635.
[8] NEESS D, BEK S, ENGELSBY H, et al. Long-chain acyl-CoA esters in metabolism and signaling:Role of acylCoA binding proteins[J]. Prog Lipid Res, 2015(59):1-25.
[9] TAKAHASHI T, GASCH A, NISHIZAWA N, et al. The DIMINUTO gene of Arabidopsis is involved in regulating cell elongation[J]. Genes and Development, 1995, 9(1):97-107.
[10] ZERENTURK E J, SHARPE L J, IKONEN E, et al. Desmosterol and DHCR24:Unexpected new directions for a terminal step in cholesterol synthesis[J]. Prog Lipid Res,2013, 52(4):666-680.
[11]周丽娜.SQLE调控ERK通路影响肺鳞癌细胞生长的机制[D].青岛:青岛大学, 2018.
[12] KERSHAW E E, FLIER J S. Adipose tissue as an endocrine organ[J]. J Clin Endocrinol Metab, 2004, 89(6):2548-2556.
[13]宋庆文.动物脂肪代谢过程中关键酶的研究进展[J].畜牧与饲料科学,2007(3):58-60.
[14] CHEN Y, RUI B B, TANG L Y, et al. Lipin family proteins-key regulators in lipid metabolism[J]. Ann Nutr Metab, 2015, 66(1):10-18.
[15] VAN HARMELEN V, RYDEN M, SJOLIN E, et al. A role of lipin in human obesity and insulin resistance:Relation to adipocyte glucose transport and GLUT4 expression[J]. J Lipid Res, 2007, 48(1):201-206.
[16] SERR J, SUH Y, LEE K. Cloning of comparative gene identification-58 gene in avian species and investigation of its developmental and nutritional regulation in chicken adipose tissue[J]. J Anim Sci, 2011, 89(11):3490-3500.
[17] FAULHABER-WALTER R, JOU W, MIZEL D, et al. Impaired glucose tolerance in the absence of adenosine A1receptor signaling[J]. Diabetes, 2011, 60(10):2578-2587.
[17] WATERHAM H R, KOSTER J, ROMEIJN G J, et al. Mutations in the 3beta-hydroxysterol Delta24-reductase gene cause desmosterolosis, an autosomal recessive disorder of cholesterol biosynthesis[J]. Am J Hum Genet, 2001, 69(4):685-694.
[18] HERZOG K, PRAS-RAVES M L, FERDINANDUSSE S,et al. Functional characterisation of peroxisomal beta-oxidation disorders in fibroblasts using lipidomics[J]. J Inherit Metab Dis, 2018, 41(3):479-487.
[19] YAGITA Y, SHINOHARA K, ABE Y, et al. Deficiency of a retinal dystrophy protein, Acyl-CoA binding domaincontaining 5(ACBD5), impairs peroxisomalβ-Oxidation of very-long-chain fatty acids[J]. J Biolo Chem, 2017,292(2):691-705.
[20] ZERENTURK E J, SHARPE L J, IKONEN E, et al. Desmosterol and DHCR24:Unexpected new directions for a terminal step in cholesterol synthesis[J]. Prog Lipid Res.2013, 52(4):666-680.
[21] ASTRUC M, TABACIK C, DESCOMPS B, et al. Squalene epoxidase and oxidosqualene lanosterol-cyclase activities in cholesterogenic and non-cholesterogenic tissues[J]. Biochim Biophys Acta, 1977, 487(1):204-211.
[22] SAWADA M, MATSUO M, HAGIHARA H, et al. Effect of FR194738, a potent inhibitor of squalene epoxidase,on cholesterol metabolism in HepG2 cells[J]. Eur J Pharmacol, 2001, 431(1):11-16.
[23] FERDINANDUSSE S, FALKENBERG K D, KOSTER J, et al. ACBD5 deficiency causes a defect in peroxisomal very long-chain fatty acid metabolism[J]. J Med Genet, 2017,54(5):330-337.