Publication
Sitagliptin treatment prevented pancreatic lesions evolution in a rat modelo f type 2 diabetes-proposal of antooxidant, antiapoptotic, anti-inflammatory and proproliferative mechanism
| dc.contributor.author | Mega, C. | |
| dc.contributor.author | Vala, Helena | |
| dc.contributor.author | Oliveira, J. | |
| dc.contributor.author | Teixeira, F. | |
| dc.contributor.author | Fernandes, R. | |
| dc.contributor.author | Teixeira-Lemos, E. | |
| dc.contributor.author | Reis, F. | |
| dc.date.accessioned | 2013-11-11T09:46:22Z | |
| dc.date.available | 2013-11-11T09:46:22Z | |
| dc.date.issued | 2013 | |
| dc.description.abstract | Background: This study aimed to elucidate mechanisms underlying the protective effects of sitagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, against pancreatic lesions, in an animal model of T2DM. Methods: Male obese diabetic ZDF (fa/fa) rats, 20-weeks-old, were treated with vehicle or sitagliptin (10mg/kg BW/day) for 6 weeks, and compared with lean control littermates (n=8/each). Biochemical parameters and lipid peroxidation were evaluated in serum/blood/tissues. Pancreatic lesions were assessed semiquantitatively by routine histopathological and PAS staining methods. Expression in mRNA of apoptotic (Bax, Bcl2, caspase 9), inflammatory (TNFα, IL-1β, IL6), proliferative (PCNA) and angiogenic (VEGF) mediators was assessed by RT-qPCR. Immunohistochemical methods were used to confirm Bax/Bcl2 protein expression. Results are means s.e.m. ANOVA and Post-hoc tests were used (P<0.05 was considered statistically significant). Results: Sitagliptin treatment of diabetic ZDF (fa/fa) rats, ameliorated biochemical serum/blood parameters, pancreatic lipid peroxidation and diabetic lesions. Immunohistochemistry confirmed antiapoptotic effect observed by reduced expression of Bax/Bcl2 ratio by RT-qPCR. Caspase 9, IL-1β mRNA expression was decreased and proliferative and angiogenic factors overexpressed. Conclusions: Sitagliptin, in this animal model of T2DM, may derive its protective pancreatic effect by antioxidant, antiapoptotic, anti-inflammatory and proproliferative/proangiogenic mechanisms. | por |
| dc.description.sponsorship | FCT/COMPETE-Strategic Project (Ref: PEst-C/SAU/UI3282/2011), PROTEC- Superior Polytechnic Institute of Viseu (ISPV) | por |
| dc.identifier.citation | C Mega, H Vala, J Oliveira, F Teixeira, R Fernandes, E Teixeira-Lemos, F Reis (2013). Sitagliptin treatment prevented pancreatic lesions evolution in a rat modelo f type 2 diabetes-proposal of antooxidant, antiapoptotic, anti-inflammatory and proproliferative mechanism. Virchows Arch 463: 157 | por |
| dc.identifier.uri | http://hdl.handle.net/10400.19/1894 | |
| dc.language.iso | eng | por |
| dc.peerreviewed | yes | por |
| dc.subject | Sitagliptin | por |
| dc.subject | Pancreatic lesions | por |
| dc.subject | At modelo type 2 | por |
| dc.subject | Antooxidant | por |
| dc.subject | Antiapoptotic | por |
| dc.subject | Anti-inflammatory | por |
| dc.subject | Proproliferative | por |
| dc.title | Sitagliptin treatment prevented pancreatic lesions evolution in a rat modelo f type 2 diabetes-proposal of antooxidant, antiapoptotic, anti-inflammatory and proproliferative mechanism | por |
| dc.type | conference object | |
| dspace.entity.type | Publication | |
| oaire.citation.conferencePlace | Lisbon, Portugal | por |
| oaire.citation.endPage | 157 | por |
| oaire.citation.startPage | 157 | por |
| oaire.citation.title | Virchows Arch | por |
| person.familyName | Vala Correia | |
| person.givenName | Helena Maria | |
| person.identifier.ciencia-id | 7A1E-E85E-FFA4 | |
| person.identifier.orcid | 0000-0001-6829-4867 | |
| rcaap.rights | openAccess | por |
| rcaap.type | conferenceObject | por |
| relation.isAuthorOfPublication | cdc3d2e2-df06-40ed-8900-1ecbc8a06c8a | |
| relation.isAuthorOfPublication.latestForDiscovery | cdc3d2e2-df06-40ed-8900-1ecbc8a06c8a |