Related Experiment Video
Updated: Dec 13, 2025

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
Role of advanced glycation end products and insulin resistance in diabetic nephropathy
Kirti Parwani1, Palash Mandal1
1Department of Biological Sciences, P. D. Patel Institute of Applied Sciences, Charotar University of Science and Technology, Changa, Gujarat 388421, India.
Abstract:
Metabolic syndrome (MetS), i.e. a cluster of physiological and biochemical abnormalities can lead to diabetic nephropathy (DN). Insulin resistance, impaired fasting glucose are the main signs and symptoms of MetS. Excess sugar can induce various substantial structural changes like formation of advanced glycation end products (AGEs). AGEs are formed due to reaction of reducing sugars with amino groups of proteins, lipids and nucleic acids. AGEs when bound to the receptor for advanced glycation end products (RAGE) activate increased production of pro-inflammatory markers like interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-α) along with induction of endoplasmic reticulum (ER) stress. Accumulation of AGEs, enhanced reactive oxygen species (ROS) generation and activation of protein kinase C (PKC), are considered to induce glomerular hypertrophy, podocyte apoptosis, therefore contributing to the development and progression of DN. In this review, we decipher different biochemical and physiological factors that link AGEs and DN.
Related Concept Videos
Diabetes Mellitus: Type 2 and Gestational
Chronic Kidney Disease I: Introduction
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
Diabetes: Symptoms, Diagnosis, and Complications
Nephrotic Syndrome I : Introduction
Oral Hypoglycemic Agents: Biguanides and Glitazones

