Full text
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| Author(s): |
Nagela Angelini
Total Authors: 1
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| Document type: | Master's Dissertation |
| Press: | Campinas, SP. |
| Institution: | Universidade Estadual de Campinas (UNICAMP). Instituto de Biologia |
| Defense date: | 2009-06-15 |
| Examining board members: |
José Roberto Bosqueiro;
Leonardo dos Reis Silveira;
Cristina Pontes Vicente
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| Advisor: | José Roberto Bosqueiro |
| Abstract | |
In adults, the beta-cell mass is maintained via a balance of beta-cell proliferation, size, neogenesis, and beta-cell death. The insulin-resistant state disrupts this regulation and alters beta-cell growth and survival, promoting a compensatory increase in beta-cell mass and insulin secretion. Here, we investigated the contribution of the cholinergic nervous system to dexamethasone-induced insulin resistance and hyperinsulinemia in rats. Seventy-day-old Wistar male rats were distributed in three groups, control (CTL), vagotomized (VAG), and sham operated (SHAM). On the 90th day of life, half of the rats were treated daily with 1 mg/kg of dexamethasone for 5 days (CTL DEX, VAG DEX, and SHAM DEX). In the presence of 8.3 mM glucose plus 100 µM carbachol (Cch), isolated islets from CTL DEX secreted significantly more insulin than CTL. No differences in insulin secretion were observed between CTL and SHAM or CTL DEX and SHAM DEX. However, islets from VAG DEX secreted significantly more insulin than SHAM DEX. Cch-potentialization of secretion was further increased in islets from VAG CTL and VAG DEX than SHAM CTL and SHAM DEX, respectively. In CTL DEX islets, M3R and PLC?1, but not PKC?, protein content was significantly higher compared with each respective control; however, pPKC? was significantly increased in the CTL DEX. In islets from VAG DEX, the expression of M3R protein increased significantly compared to VAG CTL and SHAM DEX. Vagotomy per se did not affect insulin resistance, but attenuated fasted and fed insulinemia in VAG DEX, compared with SHAM DEX rats. In conclusion, these data indicate an important participation of the cholinergic nervous system through muscaric receptors in dexamethasone-induced hyperinsulinemia in rats (AU) | |