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Effect of catch-up growth after food restriction on the entero-insular axis in rats
BACKGROUND: Catch-up growth after food restriction (CUGFR) is characterized by a significant change in food intake which could theoretically lead to the change in glucagon-like peptide-1 (GLP-1) secretion that consequently results in altered functions of pancreatic islets. METHODS: Experimental rats...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890696/ https://www.ncbi.nlm.nih.gov/pubmed/20504302 http://dx.doi.org/10.1186/1743-7075-7-45 |
Sumario: | BACKGROUND: Catch-up growth after food restriction (CUGFR) is characterized by a significant change in food intake which could theoretically lead to the change in glucagon-like peptide-1 (GLP-1) secretion that consequently results in altered functions of pancreatic islets. METHODS: Experimental rats were divided into two groups. Rats in CUGFR group were put on food-restriction for 4 weeks, and then allowed full access to food for 0, 2, 4 weeks respectively while rats in the control group were offered ad libitum access to food. Plasma glucose, insulin and GLP-1 level during OGTT were measured in all the rats. Moreover, morphology of intestinal mucosa, number of L cells, beta cell mass, incretin effect and the expression of GLP-1 receptor (GLP-1R) gene in the islets were also determined. RESULTS: The size of pancreatic islets, insulin concentration, plasma GLP-1 concentration, incretin effect, villus height-to-crypt depth ratio and L cells were all significantly decreased in CUGFR group at the end of a 4-week food-restriction period as compared with the controls. Insulin concentration and the villus height-to-crypt depth ratio were increased and finally exceeded the level of the control group over a 4-week catch-up period. Nevertheless, at the conclusion of the study, islet size, L cells number, plasma GLP-1 concentration and incretin effect increased but failed to reach the levels of the controls. CONCLUSION: CUGFR decreases incretin effect and disturbs the entero-insular axis partially by decreasing GLP-1 concentration, which might be responsible for the increased risk of metabolic disorder during CUGFR. |
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