Role of advanced glycation end products and insulin resistance in diabetic nephropathy

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 advan...

Full description

Saved in:
Bibliographic Details
Published in:Archives of physiology and biochemistry 2023-01, Vol.129 (1), p.95-107
Main Authors: Parwani, Kirti, Mandal, Palash
Format: Article
Language:English
Subjects:
Advanced glycation end products
Diabetes Mellitus
Diabetic Nephropathies - metabolism
diabetic nephropathy
endoplasmic reticulum stress
Glycation End Products, Advanced - metabolism
Humans
Insulin Resistance
Metabolic Syndrome
Reactive Oxygen Species - metabolism
receptor for advanced glycation end products
Receptor for Advanced Glycation End Products - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1381-3455
1744-4160
DOI:10.1080/13813455.2020.1797106