Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/97259
Type: Artigo de periódico
Title: Decreased β-cell Insulin Secretory Function In Aged Rats Due To Impaired Ca2+ Handling
Author: Ribeiro R.A.
Batista T.M.
Coelho F.M.
Boschero A.C.
Lopes G.S.
Carneiro E.M.
Abstract: Ageing 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 Akt1/2/3 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 [Ca2+]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 Ca2+ handling. Furthermore, the expression of proteins of the insulin transduction cascade showed an adaptive profile, with a compensatory increase in IRβ and Akt1/2/3 in gastrocnemius muscles, which may maintain normal glucose homeostasis in 24-month-old rats. © 2012 The Physiological Society.
Editor: 
Rights: fechado
Identifier DOI: 10.1113/expphysiol.2012.064790
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-84865533300&partnerID=40&md5=3356adeebeb1d3895fb7080397ef58d5
Date Issue: 2012
Appears in Collections:Unicamp - Artigos e Outros Documentos

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