title: Identification of protective components that prevent the exacerbation of goose fatty liver: Characterization, expression and regulation of adiponectin receptors.
abstract: Fat accumulation in the liver is a natural process in goose, which prepares goose for long-distance migration. In contrast to mammalian fatty liver that usually progresses into an irreversible status, steatohepatitis, goose fatty liver can return to normal without obvious pathological damage, suggesting a protective system exists in goose liver. This study was to identify the components of this system. We first focused on goose adiponectin receptor 1 and 2 (Adipor1/2) as they have ceramidase activity, and can cleave ceramide, a group of proinflammatory signaling lipid species. Quantitative analysis indicated that tumor necrosis factor alpha (Tnfα), a key proinflammatory cytokine, was down-regulated in goose fatty liver by overfeeding. This inhibition of Tnfα was accompanied with reduced adiponectin and increased Adipor1/2 in the adipose tissues and in the livers of the overfed geese, respectively. To investigate the regulation of goose Adipor2 in the context of fatty liver, we treated goose primary hepatocytes with fatty liver associated factors. Data indicated that Adipor2 was upregulated by glucose and oleate but not palmitate. Its expression was even suppressed by high level of insulin. The regulation of Adipor1 by these factors was quite similar to that of Adipor2 except that glucose did not induce Adipor1. Together, these findings suggest the upregulation of Adipor1/2 may, at least partially, contribute to the inhibition of inflammation in goose fatty liver, and the expression of Adipor1/2 can be regulated by fatty liver-associated factors.
authors.affiliation: College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China. Electronic address: tygeng@yzu.edu.cn.
authors.forename: Tuoyu
authors.initials: T
authors.lastname: Geng
authors.affiliation: College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China.
authors.forename: Biao
authors.initials: B
authors.lastname: Yang
authors.affiliation: College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China.
authors.forename: Fuyuan
authors.initials: F
authors.lastname: Li
authors.affiliation: College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Xia
authors.affiliation: College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China.
authors.forename: Qianqian
authors.initials: Q
authors.lastname: Wang
authors.affiliation: College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China.
authors.forename: Xing
authors.initials: X
authors.lastname: Zhao
authors.affiliation: College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China. Electronic address: yzgong@163.com.
authors.forename: Daoqing
authors.initials: D
authors.lastname: Gong
mesh_terms: D050153:Abdominal Fat / Q000276:immunology / Q000378:metabolism; D052242:Adiponectin / Q000235:genetics / Q000378:metabolism; D000818:Animals; D017849:Animals, Inbred Strains; D030161:Avian Proteins / Q000819:agonists / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D002681:China; D018450:Disease Progression; D004625:Embryo, Nonmammalian / Q000166:cytology; D004750:Enteral Nutrition / Q000009:adverse effects / Q000662:veterinary; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000662:veterinary*; D005777:Geese; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000009:adverse effects / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D008082:Lipotropic Agents / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D019301:Oleic Acid / Q000009:adverse effects / Q000378:metabolism; D011201:Poultry Diseases / Q000209:etiology / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D020033:Protein Isoforms / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D054419:Receptors, Adiponectin / Q000819:agonists / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D052242:Adiponectin; D030161:Avian Proteins; D007328:Insulin; D008082:Lipotropic Agents; D020033:Protein Isoforms; D054419:Receptors, Adiponectin; D014409:Tumor Necrosis Factor-alpha; D019301:Oleic Acid; D005947:Glucose
keywords: Adiponectin receptor; Fatty liver; Goose; Primary hepatocyte