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1.
Chinese Pharmacological Bulletin ; (12): 1673-1677, 2009.
Artículo en Chino | WPRIM | ID: wpr-405116

RESUMEN

Glucagon-like peptide-2 (GLP-2) is a 33-amino acid peptide derived from the tissue-specific, post-translational processing of the proglucagon gene.GLP-2 is a newly discovered,specific for the intestine growth factor that affects gastrointestinal functions including epithelial growth of normal and developing intestinal preventing damage and facilitating intestinal repair in animal models and patients of intestinal disease. GLP-2 also inhibits gastrointestinal motility and gastric acid secretion, up-regulates intestinal blood flow and reduces food intake. The actions of GLP-2 are initiated by activation of the GLP-2 receptor (GLP-2R), a specific G-protein-linked membrane receptor. This review provides an overview of the physiological, pharmacological, and therapeutic actions of GLP-2 and GLP-2R signaling mechanism, with a focus on the most recent findings on the role of this peptide hormone in the normal and diseased gastrointestinal tract.

2.
Artículo en Chino | WPRIM | ID: wpr-678577

RESUMEN

Objective To investigate the effects of glucagon like peptide 2(GLP 2) on the mRNA expressions of GLP 2 receptor (GLP 2R) and proglucagon gene(PG) in postburn rats. Methods A total of 55 Wistar rats were randomly divided into three groups including burn group, GLP 2 treatment group(treated with GLP 2, 200 ?g/kg, b.i.d ) and normal control group. Rats were sacrificed at 6, 12 h and 1, 3 and 5 d after burn injury. The proliferating cell nuclear antigen(PCNA) expression and the histological changes of the intestinal mucosa were determined by immunohistochemical staining. mRNA expressions of GLP 2R and PG were detected by RT PCR at 6, 12 h and 1, 3 and 5 d after burn injury. Results The expression of PCNA in rat intestinal mucosa decreased at 1 d after burn injury, but it was stronger in GLP 2 treatment group than that in burn group. Histological observation revealed that intestinal villi in GLP 2 treatment group were regularly arranged without obvious epithelial shedding. PG mRNA expression peaked at 12 h, 1 and 3 d after burn injury. No change of PG mRNA expression was found after treatment with GLP 2. Decreased GLP 2R mRNA expression was found in postburn rats, but after treatment with GLP 2, increased GLP 2R mRNA expression was found. Conclusion GLP 2 supplementation can keep the structure of the postburn rat intestinal mucosa without affecting PG gene expression. The mechanism may probably be related to the promotion of the mRNA expression of GLP 2R of the intestinal mucosa in rats.

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