Glucagon-Like Peptide 2 Stimulates Postresection Intestinal Adaptation in Preterm Pigs by Affecting Proteins Related to Protein, Carbohydrate, and Sulphur Metabolism
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BACKGROUND: Exogenous glucagon-like peptide 2 (GLP-2) stimulates intestinal adaptation after resection in animal models of pediatric short bowel syndrome (SBS). It is unknown whether the molecular mechanisms of such GLP-2 effects are similar to those of postresection spontaneous adaptation. Using preterm pigs as a model, we hypothesized that GLP-2 treatment would change the intestinal proteome within the first week after resection, relative to individuals not resected or resected without GLP-2 treatment.
MATERIALS AND METHODS: Two-day-old preterm pigs were subjected to resection of 50% distal small intestine and fed total parenteral nutrition without (SBS) or with GLP-2 infusion (3.5 µg/kg/h, SBS+GLP-2) for 5 days. The proteome of the remnant proximal intestine was compared among the SBS, SBS+GLP-2, and unresected pigs, through gel-based proteomics.
RESULTS: Thirty-two proteins with differential expression were identified. Ten of these proteins were affected by the resection alone (ie, SBS vs unresected pigs). Five of these resection-responsive proteins and another 22 proteins were affected by GLP-2 infusion (ie, SBS+GLP-2 vs SBS or unresected pigs). Resection alone mainly affected cellular structural proteins, while the added GLP-2 treatment affected proteins involved in protein processing and the metabolism of protein, carbohydrate, and sulphur.
CONCLUSION: In the first days following resection, proteins affected by resection plus GLP-2 treatment differed markedly from those affected by the spontaneous intestinal adaptation following resection alone. Whether more long-term GLP-2 treatment may affect the intestinal proteome following intestinal resection remains unknown.
Original language | English |
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Journal | Journal of Parenteral and Enteral Nutrition |
Volume | 41 |
Issue number | 8 |
Pages (from-to) | 1293-1300 |
Number of pages | 8 |
ISSN | 0148-6071 |
DOIs | |
Publication status | Published - 2017 |
ID: 172431205