Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/109506
Title: Sitagliptin prevents inflammation and apoptotic cell death in the kidney of type 2 diabetic animals
Authors: Marques, Catarina 
Mega, Cristina 
Gonçalves, Andreia 
Rodrigues-Santos, Paulo 
Lemos, Edite Teixeira de 
Teixeira, Frederico 
Fontes-Ribeiro, Carlos A. 
Reis, F. 
Fernandes, Rosa 
Issue Date: 2014
Publisher: Hindawi
Project: PEst-C/SAU/UI3282/2011 
PEst- C/SAU/UI3282/2013 
Serial title, monograph or event: Mediators of Inflammation
Volume: 2014
Abstract: This study aimed to evaluate the efficacy of sitagliptin, a dipeptidyl peptidase IV (DPP-IV) inhibitor, in preventing the deleterious effects of diabetes on the kidney in an animal model of type 2 diabetes mellitus; the Zucker diabetic fatty (ZDF) rat: 20-week-old rats were treated with sitagliptin (10 mg/kg bw/day) during 6 weeks. Glycaemia and blood HbA1c levels were monitored, as well as kidney function and lesions. Kidney mRNA and/or protein content/distribution of DPP-IV, GLP-1, GLP-1R, TNF-α, IL-1β, BAX, Bcl-2, and Bid were evaluated by RT-PCR and/or western blotting/immunohistochemistry. Sitagliptin treatment improved glycaemic control, as reflected by the significantly reduced levels of glycaemia and HbA1c (by about 22.5% and 1.2%, resp.) and ameliorated tubulointerstitial and glomerular lesions. Sitagliptin prevented the diabetes-induced increase in DPP-IV levels and the decrease in GLP-1 levels in kidney. Sitagliptin increased colocalization of GLP-1 and GLP-1R in the diabetic kidney. Sitagliptin also decreased IL-1β and TNF-α levels, as well as, prevented the increase of BAX/Bcl-2 ratio, Bid protein levels, and TUNEL-positive cells which indicates protective effects against inflammation and proapoptotic state in the kidney of diabetic rats, respectively. In conclusion, sitagliptin might have a major role in preventing diabetic nephropathy evolution due to anti-inflammatory and antiapoptotic properties.
URI: https://hdl.handle.net/10316/109506
ISSN: 0962-9351
1466-1861
DOI: 10.1155/2014/538737
Rights: openAccess
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais
FMUC Medicina - Artigos em Revistas Internacionais

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