Protein deficiency and nutritional recovery modulate insulin secretion and the early steps of insulin action in rats

dc.contributor.authorLatorraca, Márcia Q.
dc.contributor.authorReis, Marise A. B.
dc.contributor.authorCarneiro, Everardo M. [UNESP]
dc.contributor.authorMello, Maria A. R. [UNESP]
dc.contributor.authorVelloso, Licio A.
dc.contributor.authorSaad, Mario J. A.
dc.contributor.authorBoschero, A. Carlos
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de Mato Grosso
dc.description.abstractMaternal malnutrition was shown to affect early growth and leads to permanent alterations in insulin secretion and sensitivity of offspring. In addition, epidemiological studies showed an association between low birth weight and glucose intolerance in adult life. To understand these interactions better, we investigated the insulin secretion by isolated islets and the early events related to insulin action in the hind-limb muscle of adult rats fed a diet of 17% protein (control) or 6% protein [low (LP) protein] during fetal life, suckling and after weaning, and in rats receiving 6% protein during fetal life and suckling followed by a 17% protein diet after weaning (recovered). The basal and maximal insulin secretion by islets from rats fed LP diet and the basal release by islets from recovered rats were significantly lower than that of control rats. The dose-response curves to glucose of islets from LP and recovered groups were shifted to the right compared to control islets, with the half-maximal response (EC 50) occurring at 16.9 ± 1.3, 12.4 ± 0.5 and 8.4 ± 0.1 mmol/L, respectively. The levels of insulin receptor, as well as insulin receptor substrate-1 and phosphorylation and the association between insulin receptor substrate-1 and phosphatidylinositol 3-kinase were greater in rats fed a LP diet than in control rats. In recovered rats, these variables were not significantly different from those of the other two groups. These results suggest that glucose homeostasis is maintained in LP and recovered rats by an increased sensitivity to insulin as a result of alterations in the early steps of the insulin signal transduction pathway.en
dc.description.affiliationDepto. de Fisiologia e Biofisica Instituto de Biologia Universidade Estadual de Campinas, Campinas, São Paulo 13083-970
dc.description.affiliationDepto. de Educ. Física Instituto de Biociências Universidade Estadual Paulista, Rio Claro, São Paulo 13506-900
dc.description.affiliationDepto. de Clin. Médica Faculdade de Cie. Médicas Universidade Estadual de Campinas, Campinas, São Paulo, 13081-970
dc.description.affiliationUniversidade Federal de Mato Grosso, Cuiabá, MT
dc.description.affiliationUnespDepto. de Educ. Física Instituto de Biociências Universidade Estadual Paulista, Rio Claro, São Paulo 13506-900
dc.identifier.citationJournal of Nutrition, v. 128, n. 10, p. 1643-1649, 1998.
dc.relation.ispartofJournal of Nutrition
dc.rights.accessRightsAcesso restrito
dc.subjectInsulin receptor
dc.subjectInsulin receptor substrate- 1
dc.subjectInsulin secretion
dc.subjectNutritional recovery
dc.subjectinsulin receptor
dc.subjectinsulin receptor substrate 1
dc.subjectphosphatidylinositol 3 kinase
dc.subjectanimal tissue
dc.subjectdisease association
dc.subjectdose response
dc.subjectglucose homeostasis
dc.subjectglucose intolerance
dc.subjectglucose tolerance test
dc.subjectinsulin release
dc.subjectinsulin sensitivity
dc.subjectinsulin tolerance test
dc.subjectlow birth weight
dc.subjectpancreas islet cell
dc.subjectprotein deficiency
dc.subjectprotein diet
dc.subjectprotein restriction
dc.subjectsignal transduction
dc.subjectBlood Glucose
dc.subjectDietary Proteins
dc.subjectIslets of Langerhans
dc.subjectMaternal-Fetal Exchange
dc.subjectProtein Deficiency
dc.subjectRats, Wistar
dc.titleProtein deficiency and nutritional recovery modulate insulin secretion and the early steps of insulin action in ratsen
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Rio Claropt