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Association of selenoprotein gene expression with pancreatic atrophy in broiler chicks
Author(s) -
Li Dai-Lin,
Huang Jia-Qiang,
Zhao Hua,
Xia Xin-Jie,
Wang Kang- Ning,
Lei Xin Gen
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.241.8
Subject(s) - selenoprotein , endocrinology , medicine , biology , pancreas , acinar cell , selenium deficiency , atrophy , selenoprotein p , pathogenesis , gene expression , gene , oxidative stress , genetics , superoxide dismutase , glutathione peroxidase
Pancreatic atrophy is one of the classical Se‐deficiency diseases in chicks, but the pathological mechanism remains unclear. Our objective was to replicate this disease to study novel roles and mechanisms of selenoproteins in its pathogenesis. Four groups of day‐old chicks (n=60/group) were fed a corn‐soy basal diet (BD, 14 μg Se/kg) or the BD + all‐rac‐α‐tocopheryl acetate at 50 mg/kg, Se (as sodium selenite) at 0.3 mg/kg, or both for 4 wk. Acinar pancreatic degeneration was seen in chicks fed the BD. Pancreatic length was decreased (P < 0.05) by both Se and vitamin E deficiencies, whereas pancreatic weight was decreased (P < 0.05) by only the Se deficiency. Among 15 selenoprotein genes assayed in pancreas, 11, 9, and 11 genes were affected (P < 0.05) by Se, vitamin E, and their interactions, respectively. Gene expression of 3 key transcriptional factors ( Pdx1, Mafa, and Foxa2 ) for pancreatic development and differentiation was down‐regulated (P < 0.05) by Se or vitamin E deficiency. While pancreatic mRNA levels of a key cell‐proliferation factor ( Tgfb2 ) were decreased (P < 0.05) by the Se deficiency, gene expression of 2 cell death‐related factors ( Casp3 and p53 ) was affected (P < 0.05) by the interactions of the two nutrients. In conclusion, pancreatic atrophy was experimentally induced in chicks to show association of multiple selenoprotein gene expressions with the disease. (NSFC; Chang Jiang Scholars; NIH 53018).