Study of diabetic bladder dysfunction in leptin-deficient mice (ob/ob): impact of chronic methylglyoxal administration

• Grant number: 25/10412-1
• Support Opportunities: Scholarships in Brazil - Master
• Start date: July 01, 2025
• End date: June 30, 2026
• Field of knowledge: Biological Sciences - Pharmacology
• Principal Investigator: Edson Antunes
• Grantee: Clarissa Paiva Horioka
• Host Institution: Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Associated research grant: 24/10306-4 - Methylglyoxal - advanced glycation end products (AGEs) - receptor for AGEs (AGEr) axis: A potential therapeutical target for prevention and treatment of bladder dysfunction associated with obesity and diabetes, AP.R

Abstract

Diabetes mellitus (DM) is a metabolic syndrome characterized by high blood glucose levels. One of its complications is diabetic bladder dysfunction (DBD), which affects over 50% of diabetic patients. Problems related to the lower urinary tract in DBD are significant, and although voiding changes are not life-threatening, they can substantially impact individuals' quality of life and contribute to high healthcare costs. Methylglyoxal (MGO) is a dicarbonyl compound found in elevated levels in the blood of diabetic patients. MGO-induced glycation of macromolecules leads to the formation of advanced glycation end products (AGEs), which interact with their AGEr receptors, resulting in increased reactive oxygen species (ROS) production and inflammation. Our research group has been emphasizing the role of MGO in bladder dysfunction, and in this project, we aim to further understand the MGO-AGEs-AGEr-ROS pathway in DBD regulation. Specifically, we will investigate whether the consumption of exogenous MGO (primarily present in processed foods) exacerbates bladder dysfunction in type 2 diabetic models, as this animal model already exhibits high endogenous AGE levels due to hyperglycemia. (AU)