Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/194011
Type: Artigo de periódico
Title: Glucose-induced Insulin Secretion Is Impaired And Insulin-induced Phosphorylation Of The Insulin Receptor And Insulin Receptor Substrate-1 Are Increased In Protein-deficient Rats.
Author: Reis, M A
Carneiro, E M
Mello, M A
Boschero, A C
Saad, M J
Velloso, L A
Abstract: Malnutrition is related to diabetes in tropical countries. In experimental animals, protein deficiency may affect insulin secretion. However, the effect of malnutrition on insulin receptor phosphorylation and further intracellular signaling events is not known. Therefore, we decided to evaluate the rate of insulin secretion and the early molecular steps of insulin action in insulin-sensitive tissues of an animal model of protein deficiency. Pancreatic islets isolated from rats fed a standard (17%) or a low (6%) protein diet were studied for their secretory response to increasing concentrations of glucose in the culture medium. Basal as well as maximal rates of insulin secretion were significantly lower in the islets isolated from rats fed a low protein diet. Moreover, the dose-response curve to glucose was significantly shifted to the right in the islets from malnourished rats compared with islets from control rats. During an oral glucose tolerance test, there were significantly lower circulating concentrations of insulin in the serum of rats fed a low protein diet in spite of no difference in serum glucose concentration between the groups, suggesting an increased peripheral insulin sensitivity. Immunoblotting and immunoprecipitation were used to study the phosphorylation of the insulin receptor and the insulin receptor substrate-1 as well as the insulin receptor substrate-1-p85 subunit of phosphatidylinositol 3-kinase association in response to insulin. Values were greater in hind-limb muscle from rats fed a low protein diet compared with controls. No differences were detected in the total amount of protein corresponding to the insulin receptor or insulin receptor substrate-1 between muscle from rats fed the two diets. Therefore, we conclude that a decreased glucose-induced insulin secretion in pancreatic islets from protein-malnourished rats is responsible, at least in part, for an increased phosphorylation of the insulin receptor, insulin receptor substrate-1 and its association with phosphatidylinositol 3-kinase. These might represent some of the factors influencing the equilibrium in glucose concentrations observed in animal models of malnutrition and undernourished subjects.
Subject: Animals
Dose-response Relationship, Drug
Glucose
Glucose Tolerance Test
Immunoblotting
Insulin
Insulin Receptor Substrate Proteins
Islets Of Langerhans
Male
Muscle, Skeletal
Phosphoproteins
Phosphorylation
Precipitin Tests
Protein Deficiency
Protein-energy Malnutrition
Rats
Rats, Wistar
Receptor, Insulin
Rights: fechado
Identifier DOI: 
Address: http://www.ncbi.nlm.nih.gov/pubmed/9082023
Date Issue: 1997
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

Files in This Item:
File SizeFormat 
pmed_9082023.pdf670.84 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.