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Role of I / D polymorphism of the ACE gene and diabetes on the renin-angiotensin and kallikrein kinin systems in renal tissue

Grant number: 11/14548-2
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): December 01, 2011
Effective date (End): August 31, 2013
Field of knowledge:Health Sciences - Medicine
Principal researcher:Dulce Elena Casarini
Grantee:Nádia de Sousa da Cunha Bertoncello
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
Associated research grant:10/51904-9 - Renin angiotensin and kallikrein kinin systems in hypertension, obesity, diabetes, desnutrition and sepsis: molecular, cellular and physiopathologic mechanisms, AP.TEM


In recent years, much effort has been directed not only to understanding the human genome, but also to the investigation of candidate genes that may influence the development or progression of frequent and complex human disorders such as cancer, hypertension and diabetes mellitus (DM). It is known that diabetic nephropathy affects 30-50% of type I diabetic patients, and approximately 10-40% of type II diabetics who manifest the disease for more than 10-20 years. This complication is a major cause of end stage renal disease (ESRD), increasing by at least three times the risk for developing cardiovascular disease in these patients. It has been shown that chronic hyperglycemia is not the only cause responsible for renal complications, and genetic factors play an important role. In this sense, population studies in families show a strong association between diabetic nephropathy and the polymorphism of insertion / deletion (I / D) in intron 16 of the gene for angiotensin-converting enzyme (ACE), resulting in differences in plasma and tissue ACE (I / I, 76%, I / D, 100% D / D, 126% on average). Furthermore, studies have shown that the renin angiotensin system (RAS) present within the glomeruli and proximal tubules can be activated by hyperglycemia, leading to increased synthesis of angiotensin II. On the other hand, it is known that bradykinin (1-9) modulates the effects caused by angiotensin II and thus, because of an imbalance between the RAS and kallikrein-kinin system, bradykinin may be involved in the installation and development of diabetic nephropathy. Therefore, the purpose of this study is to evaluate in vivo the interaction between high glucose and the polymorphism I/D of ACE gene, as well as the influence of both on the components of the RAS and bradykinin in the kidney, contributing to the understanding of the mechanisms involved in the process of glomerular sclerosis and optimization of patient care. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
BERTONCELLO, NADIA; MOREIRA, ROSELI PERES; ARITA, DANIELLE YURI; ARAGAO, DANIELLE S.; MIZUNO WATANABE, INGRID KAZUE; DANTAS, PATRICIA S.; SANTOS, RALMONY; MATTAR-ROSA, RODOLFO; YOKOTA, RODRIGO; CUNHA, TATIANA SOUSA; et al. Diabetic Nephropathy Induced by Increased Ace Gene Dosage Is Associated with High Renal Levels of Angiotensin (1-7) and Bradykinin. JOURNAL OF DIABETES RESEARCH, . (11/14548-2, 10/51904-9)

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