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Glucagon‐like peptide 2 and epidermal growth factor promote intestinal adaptation in two neonatal intestinal failure models
Author(s) -
Koepke Jacob,
Lim David,
Wales Paul,
Wizzard Pamela,
Sigalet David,
Li Julang,
Turner Justine,
Levesque Crystal
Publication year - 2015
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.29.1_supplement.265.1
Subject(s) - glucagon like peptide 2 , epidermal growth factor , short bowel syndrome , medicine , endocrinology , claudin , ileum , cdx2 , saline , gene expression , biology , tight junction , receptor , microbiology and biotechnology , peptide , gene , parenteral nutrition , biochemistry , homeobox
This study assessed the efficacy of exogenous GLP‐2 and EGF therapy, alone and in combination, on ileal gene expression in two translational piglet models of neonatal short bowel syndrome: a 75% mid‐intestinal resection (JI model) or a 75% distal‐intestinal resection including removal of the ileo‐cecal junction (JC model). JI and JC piglets (age 3‐5 days) received one of 4 treatments (saline, GLP‐2, EGF and GLP‐2+EGF) for 7 days after surgical modification. Expression of genes related to tissue repair (trefoil factor 3, TTF3), cell proliferation (ki‐67), differentiation (cdx2), and apoptosis (caspase 3, c3), digestive enzymes (intestinal alkaline phosphatase, IAP), and tight junction proteins (claudin 7 and 15) were assessed. The CONTRAST statement was used to compare the saline with the treatment groups within each model. In JI pigs, administration of GLP‐2 and EGF, alone or in combination increased (p<0.05) expression of TFF3 and claudin ‐7 and ‐15 and tended to increase (p=0.08) IAP expression. There was no effect of treatment on ki‐67, cdx2, or c3 expression. In JC pigs, administration of GLP‐2 and EGF, alone or in combination tended to increase (p=0.06) expression of TTF3 and claudin‐15 but there was no effect of treatment on expression of on ki‐67, cdx2, IAP, c3, or claudin‐7 expression. Regardless of the surgical model, GLP‐2 and EGF therapy promote tissue repair and barrier function.