Decreased β-cell Insulin Secretory Function In Aged Rats Due To Impaired Ca(2+) Handling.

dc.creatorRibeiro, Rosane Aparecida
dc.creatorBatista, Thiago Martins
dc.creatorCoelho, Fernanda Monteiro
dc.creatorBoschero, Antonio Carlos
dc.creatorLopes, Guiomar Silva
dc.creatorCarneiro, Everardo Magalhães
dc.date2012-Sep
dc.date2015-11-27T13:28:29Z
dc.date2015-11-27T13:28:29Z
dc.date.accessioned2018-03-29T01:15:16Z
dc.date.available2018-03-29T01:15:16Z
dc.identifierExperimental Physiology. v. 97, n. 9, p. 1065-73, 2012-Sep.
dc.identifier1469-445X
dc.identifier10.1113/expphysiol.2012.064790
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/22542614
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/199986
dc.identifier22542614
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1300219
dc.descriptionAgeing is associated with an increased impairment in glucose homeostasis and an increased incidence of type 2 diabetes. In this study, we evaluated β-cell function and its implications for glucose homeostasis in 24-month-old female Wistar rats. Aged rats showed lower plasma glucose levels in the fed and fasting states compared with control rats. In addition, insulinaemia in the fed state was reduced in the older rats. Insulin receptor β (IRβ) expression was lower in the livers of the aged animals, whereas IRβ and Akt(1/2/3) protein expressions were higher in the muscles. These effects may contribute to the normal glucose tolerance observed in older rodents. Isolated islets from aged rats secreted less insulin in response to 8.3 and 16.7 mm glucose. Accordingly, this group presented a lower [Ca(2+)](i) in the presence of glucose and a depolarizing stimulus (30 mm K(+)). In addition, islets from aged rats showed reduced insulin secretion in response to 100 μm carbachol (CCh), 10 nm phorbol 12-myristate 13-acetate and 10 μm forskolin. The expressions of protein kinase C, protein kinase A and exocytotic proteins, such as syntaxin 1 and synaptosomal-associated protein 25 kDa (SNAP-25), were similar in islets from aged and control rats. In conclusion, our evidence suggests that the increased incidence of type 2 diabetes with age may be due to a progressive decline in β-cell secretory capacity due to disruption of Ca(2+) handling. Furthermore, the expression of proteins of the insulin transduction cascade showed an adaptive profile, with a compensatory increase in IRβ and Akt(1/2/3) in gastrocnemius muscles, which may maintain normal glucose homeostasis in 24-month-old rats.
dc.description97
dc.description1065-73
dc.languageeng
dc.relationExperimental Physiology
dc.relationExp. Physiol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAging
dc.subjectAnimals
dc.subjectBlood Glucose
dc.subjectCalcium
dc.subjectCarbachol
dc.subjectCyclic Amp-dependent Protein Kinases
dc.subjectDiabetes Mellitus, Type 2
dc.subjectFasting
dc.subjectFemale
dc.subjectGlucose
dc.subjectInsulin
dc.subjectInsulin-secreting Cells
dc.subjectIslets Of Langerhans
dc.subjectLiver
dc.subjectMuscles
dc.subjectProtein Kinase C
dc.subjectProto-oncogene Proteins C-akt
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReceptor, Insulin
dc.subjectSynaptosomal-associated Protein 25
dc.titleDecreased β-cell Insulin Secretory Function In Aged Rats Due To Impaired Ca(2+) Handling.
dc.typeArtículos de revistas


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