[1] DAVAIL S,GUY G,ANDRE J,et al.Metabolism in two breeds of geese with moderate or large overfeeding induced liver-steatosis[J].Comparative Biochemistry and Physiology A:Molecular & Integrative Physiology,2000,126(1):91-99.

[2] KAROUSA M M,MAHMOUD E A,ELIETHY S M,et al.Effect of forced-feeding on the growth performance and liver quality of egyptian geese[J].Benha Veterinary Medical Journal,2013,24(1):254-260.
[3] FRANCQUE S,DER GRAAFF D V,KWANTEN W J,et al.Non-alcoholic fatty liver disease and cardiovascular risk:pathophysiological mechanisms and implications[J].Journal of Hepatology,2016,65(2):425-443.

[4] HERMIER D,SALICHON M R,GUY G,et al.Differential channelling of liver lipids in relation to susceptibility to hepatic steatosis in the goose[J].Poultry Science,1999,78(10):1398-1406.

[5] HERMIER D,ROUSSELOTPAILLEY D,PERESSON R,et al.Influence of orotic acid and estrogen on hepatic lipid storage and secretion in the goose susceptible to liver steatosis[J].Biochimica et Biophysica Acta,1994,1211(1):97-106.

[6] HERMIER D,SAADOUN A,SALICHON M R,et al.Plasma lipoproteins and liver lipids in two breeds of geese with different susceptibility to hepatic steatosis:changes induced by development and force-feeding[J].Lipids,1991,26(5):331-339.

[7] GENG T,HU W,BROADWATER M H,et al.Fatty acids differentially regulate insulin resistance through endoplasm reticulum stress-mediated induction of tribbles homologue 3:a potential link between dietary fat composition and the pathophysiological outcomes of obesity[J].Diabetologia,2013,56(9):2078-2087.

[8] LIU D,HAN C,WAN H,et al.Effects of inhibiting PI3K-Akt-mTOR pathway on lipid metabolism homeostasis in goose primary hepatocytes[J].Animal,2016,10(8):1319-1327.

[9] UTZSCHNEIDER K M,KAHN S E.The role of insulin resistance in nonalcoholic fatty liver disease[J].The Journal of Clinical Endocrinology and Metabolism,2006,91(12):4753-4761.

[10] GENG T,XIA L,LI F,et al.The role of endoplasmic reticulum stress and insulin resistance in the occurrence of goose fatty liver[J].Biochemical and Biophysical Research Communications,2015,465(1):83-87.

[11] WEI Y,WANG D,TOPCZEWSKI F,et al.Saturated fatty acids induce endoplasmic reticulum stress and apoptosis independently of ceramide in liver cells[J].American Journal of Physiology:Endocrinology and Metabolism,2006,291(2).
[12] GENG T,ZHAO X,XIA L,et al.Supplementing dietary sugar promotes endoplasmic reticulum stress-independent insulin resistance and fatty liver in goose[J].Biochemical and Biophysical Research Communications,2016,476(4):665-669.

[13] WEI S,HAN C,HE F,et al.Inhibition of PI3K-Akt-mTOR signal pathway dismissed the stimulation of glucose on goose liver cell growth[J].Journal of Animal Physiology and Animal Nutrition,2017,101(5):e133-e143.
[14] HAN C C,WE S H,HE F,et al.Glucose-induced lipid deposition in goose primary hepatocytes is dependent on the PI3K-Akt-mTOR signaling pathway[J].Archives of Biological Sciences,2016,68(4):853-861.

[15] WITTEVEEN M,BROWN M R,DOWNS C T,et al.Does sugar content matter? Blood plasma glucose levels in an occasional and a specialist avian nectarivore[J].Comparative Biochemistry and Physiology A:Molecular & Integrative Physiology,2014:40-44.
[16] HAN C C,WEI S H,SONG Q,et al.Insulin stimulates goose liver cell growth by activating PI3K-AKT-mTOR signal pathway[J].Cellular Physiology and Biochemistry,2016,38(2):558-570.

[17] LU L,CHEN Y,WANG Z,et al.The goose genome sequence leads to insights into the evolution of waterfowl and susceptibility to fatty liver[J].Genome Biology,2015,16(1):89-89.

[18] ZHU L H,MENG H,DUAN X J,et al.Gene expression profile in the liver tissue of geese after overfeeding[J].Poultry Science,2011,90(1):107-117.

[19] OSMAN R H,SHAO D,LIU L,et al.Expression of mitochondria-related genes is elevated in overfeeding-induced goose fatty liver[J].Comparative Biochemistry and Physiology B:Biochemistry and Molecular Biology,2016:30-37.
[20] CHEN F,ZHANG H,LI J,et al.Identification of differentially expressed miRNAs in the fatty liver of Landes goose (
Anser anser)[J].Scientific Reports,2017,7(1):16296.
[21] ZHANG J,WANG Q,ZHAO X,et al.MicroRNA-122 targets genes related to goose fatty liver[J/OL].Poultry Science,(2017-01-07)[2017-11-12],https://www.researchgate.net/publication/321234780
[22] TILG H, MOSCHEN A R.Evolution of inflammation in nonalcoholic fatty liver disease:the multiple parallel hits hypothesis[J].Hepatology,2010,52(5):1836-1846.

[23] WANG Y,WANG X,LAU W B,et al.Adiponectin inhibits tumor necrosis factor-α-induced vascular inflammatory response via caveolin-mediated ceramidase recruitment and activation[J].Circulation Research,2014,114(5):792-805.

[24] ARITA Y.Reprint of "paradoxical decrease of an adipose-specific protein, adiponectin, in obesity"[J].Biochemical and Biophysical Research Communications,2012,425(3):560-564.

[25] ALAAEDDINE N,SIDAOUI J,HILAL G,et al.TNF-α messenger ribonucleic acid (mRNA) in patients with nonalcoholic steatohepatitis[J].European Cytokine Network,2012,23(3):107-111.
[26] GENG T,YANG B,LI F,et al.Identification of protective components that prevent the exacerbation of goose fatty liver:characterization, expression and regulation of adiponectin receptors[J].Comparative Biochemistry and Physiology B,2016:32-38.
[27] RAMACHANDRAN R,OCÍN-GROVE OM,METZGER SL.Molecular cloning and tissue expression of chicken adipor 1 and adipor 2 complementary deoxyribonucleic acids[J].Domestic Animal Endocrinology,2007,33(1):19-31.

[28] SCHWARTZ E A,ZHANG W,KARNIK S K,et al.Nutrient modification of the innate immune response a novel mechanism by which saturated fatty acids greatly amplify monocyte inflammation[J].Arteriosclerosis,Thrombosis and Vascular Biology,2010,30(4):802-808.

[29] HOLLAND W L,MILLER R A,WANG Z V,et al.Receptor-mediated activation of ceramidase activity initiates the pleiotropic actions of adiponectin[J].Nature Medicine,2011,17(1):55-63.

[30] XU A,WANG Y,KESHAW H,et al.The fat-derived hormone adiponectin alleviates alcoholic and nonalcoholic fatty liver diseases in mice[J].Journal of Clinical Investigation,2003,112(1):91-100.

[31] PHIELER J,GARCIAMARTIN R,LAMBRIS J D,et al.The role of the complement system in metabolic organs and metabolic diseases[J].Seminars in Immunology,2013,25(1):47-53.

[32] PRITCHARD M T,MCMULLEN M R,STAVITSKY A B,et al.Differential contributions of C3,C5,and decay-accelerating factor to ethanol-induced fatty liver in mice[J].Gastroenterology,2007,132(3):1117-1126.

[33] LIU L,ZHAO X,WANG Q,et al.Prosteatotic and protective components in a unique model of fatty liver:gut microbiota and suppressed complement system[J].Scientific Reports,2016,6(1):43-49.
[34] RITZE Y,BARDOS G,CLAUS A,et al.Lactobacillus rhamnosus GG protects against non-alcoholic fatty liver disease in mice[J].PLoS One,2014,9(1):453-463.
[35] KELISHADI R,FARAJIAN S,MIRLOHI M,et al.Probiotics as a novel treatment for non-alcoholic fatty liver disease; a systematic review on the current evidences[J].Hepatitis Monthly,2013,13(4):1-8.
[36] 刘龙,王倩,许程,等.鹅肥肝形成中补体受体1基因的表达和调控研究[J].中国家禽,2016,38(24):5-10.
[37] MIURA K,OHNISHI H.Role of gut microbiota and Toll-like receptors in nonalcoholic fatty liver disease[J].World Journal of Gastroenterology,2014,20(23):7381-7391.

[38] SZABO G.Gut-liver axis in alcoholic liver disease[J].Gastroenterology,2015,148(1):30-36.

[39] ARONWISNEWSKY J,GABORIT B,DUTOUR A,et al.Gut microbiota and non-alcoholic fatty liver disease:new insights[J].Clinical Microbiology and Infection,2013,19(4):338-348.

[40] 杨林辉,蔡俊,陈东风.非酒精性脂肪性肝炎患者肠道菌群的变化及意义[J].临床肝胆病杂志,2012,28(2):124-126.
[41] NIELSEN T,QIN J,PRIFTI E,et al.Richness of human gut microbiome correlates with metabolic markers[J].Nature,2013,500(7464):541-546.

[42] COTILLARD A,KENNEDY S,KONG L C,et al.Dietary intervention impact on gut microbial gene richness[J].Nature,2013,500(7464):585-588.

[43] 刘龙,龚晗,杨彪,等.鹅肥肝形成中肠道生理指标、菌群及代谢物的变化[J].扬州大学学报(农业与生命科学版),2016,37(4):37-42.
[44] GUO Z,LIU X,ZHANG Q,et al.Influence of consumption of probiotics on the plasma lipid profile:A meta-analysis of randomised controlled trials[J].Nutrition Metabolism and Cardiovascular Diseases,2011,21(11):844-850.

[45] ARSLAN N.Obesity, fatty