title: Ceramide accumulation and up-regulation of proinflammatory interleukin-1β exemplify lipotoxicity to mediate declines of reproductive efficacy of broiler hens.
abstract: The study was conducted to delineate fundamental mechanisms that initiate the deleterious effect of fuel overloading on reproductive efficacy of broiler breeder hens. Sixty hens at age 26 wk were fed recommended amounts of feed (160 g/d per hen) or allowed voluntary feeding (approximately 30% more than restriction). At age 35 and 50 wk, hens were sampled for further analyzes. Voluntary feeding resulted in poor egg production, high rate of mortality, and abnormal ovarian structure (mainly overt hierarchical follicle atresia at age 35 wk and ovarian involution at age 50 wk). In contrast to feed-restricted hens, voluntary feeding also induced metabolic dysregulations that comprised enhanced adiposity; hepatic triacylglycerol accumulation; and elevated concentrations of plasma glucose, NEFAs, very low density lipoprotein, triacylglycerol, phospholipids, and sphingomyelin (P < 0.05). Furthermore, hepatic and circulating ceramide and sphingomyelin accumulation, and up-regulation of proinflammatory IL-1β expression in liver and adipose tissues (P < 0.05) systemically manifested the development of lipotoxicity in feed-satiated hens. Lipotoxicity leading to impaired ovarian dysfunctions, including follicle atresia, ovarian regression, and a decline of circulating estradiol levels (P < 0.05) in feed-satiated hens, was further exemplified by ceramide accumulation and up-regulation of IL-1β, serine palmitoyltransferase, and sphingomyelinase transcript abundance, but suppressed protein kinase Akt activation (P < 0.1 to 0.05) within the hierarchical follicles. This study provides the first in vivo evidence of the actions of ceramide and IL-1β in mediating overfeeding-induced follicle atresia and progression of ovarian involution in broiler hens.
authors.affiliation: Department of Animal Science, National Chung Hsing University, Taichung, Taiwan.
authors.forename: Y-E
authors.initials: YE
authors.lastname: Pan
authors.forename: Z-C
authors.initials: ZC
authors.lastname: Liu
authors.forename: C-J
authors.initials: CJ
authors.lastname: Chang
authors.forename: Y-L
authors.initials: YL
authors.lastname: Xie
authors.forename: C-Y
authors.initials: CY
authors.lastname: Chen
authors.forename: C-F
authors.initials: CF
authors.lastname: Chen
authors.forename: R L
authors.initials: RL
authors.lastname: Walzem
authors.forename: S-E
authors.initials: SE
authors.lastname: Chen
mesh_terms: D000273:Adipose Tissue / Q000737:chemistry; D050154:Adiposity / Q000502:physiology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002518:Ceramides / Q000032:analysis / Q000378:metabolism*; D002645:Chickens / Q000254:growth & development* / Q000378:metabolism; D004958:Estradiol / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005298:Fertility / Q000502:physiology*; D005496:Follicular Atresia; D005502:Food / Q000009:adverse effects*; D053583:Interleukin-1beta / Q000096:biosynthesis*; D008079:Lipoproteins, VLDL / Q000097:blood; D008099:Liver / Q000737:chemistry; D008659:Metabolic Diseases / Q000378:metabolism; D010053:Ovary / Q000378:metabolism / Q000503:physiopathology; D010743:Phospholipids / Q000097:blood; D010727:Phosphoric Diester Hydrolases / Q000097:blood; D051057:Proto-Oncogene Proteins c-akt / Q000096:biosynthesis; D051102:Serine C-Palmitoyltransferase / Q000096:biosynthesis; D013108:Sphingomyelin Phosphodiesterase / Q000096:biosynthesis; D014280:Triglycerides / Q000032:analysis; D015854:Up-Regulation
chemical_list: D001786:Blood Glucose; D002518:Ceramides; D005230:Fatty Acids, Nonesterified; D053583:Interleukin-1beta; D008079:Lipoproteins, VLDL; D010743:Phospholipids; D014280:Triglycerides; D004958:Estradiol; D051102:Serine C-Palmitoyltransferase; D051057:Proto-Oncogene Proteins c-akt; D010727:Phosphoric Diester Hydrolases; D013108:Sphingomyelin Phosphodiesterase; C055160:sphingomyelin phosphodiesterase D