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Vagal afferents are essential for resection‐induced intestinal growth in association with GLP‐2‐induced activation of vagal afferents in the nucleus tract solitary (NTS)
Author(s) -
Nelson David W,
Liu Xiaowen,
Raybould Helen,
Ney Denise M
Publication year - 2006
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.20.4.a548-b
Subject(s) - capsaicin , proglucagon , glucagon like peptide 2 , endocrinology , medicine , ileum , chemistry , vagus nerve , glucagon like peptide 1 , stimulation , receptor , peptide , biochemistry , type 2 diabetes , diabetes mellitus
Background & Aim The intestinal adaptive response to mid small bowel resection (SBR) involves neural pathways and enterotrophic hormones such as glucagon‐like peptide (GLP)‐2. Our aim was to test if vagal afferents are essential for resection‐induced growth, and to quantify neural activity in the NTS, the site of termination of vagal afferents, after treatment with exogenous GLP‐2. Methods Rats were treated with perivagal capsaicin (1%) or vehicle 10 d prior to experiments. Exp 1: rats received 70% SBR or transection control surgery and were fed chow for 7 d. Growth of residual bowel was assessed by changes in mucosal mass, protein, and DNA. Exp 2: Fos protein in NTS neurons was determined by immunocytochemistry after GLP‐2 (200ug) or saline, in vehicle or capsaicin‐treated rats. Results Residual ileum showed the greatest resection‐induced growth. Perivagal capsaicin attenuated gut growth by 48‐100% without attenuating increases in ileal proglucagon mRNA expression or plasma bioactive GLP‐2. GLP‐2 caused a 5‐fold increase in Fos expression, which was completely abolished by perivagal capsaicin treatment. Conclusion Attenuation of resection‐induced gut growth by capsaicin with no decrease in ileal proglucagon mRNA or plasma bioactive GLP‐2 suggests capsaicin inhibits growth by blocking GLP‐2 action. The absence of c‐Fos positive cells in the NTS of capsaicin‐treated rats implies that GLP‐2 signaling involves activation of vagal afferents. Supported by NIDDK RO1‐42835 + T32‐07665

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