Role of advanced glycation end products and insulin resistance in diabetic nephropathy.
Kirti ParwaniPalash MandalPublished in: Archives of physiology and biochemistry (2020)
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.
Keyphrases
- diabetic nephropathy
- insulin resistance
- metabolic syndrome
- reactive oxygen species
- endoplasmic reticulum
- protein kinase
- cell death
- rheumatoid arthritis
- adipose tissue
- type diabetes
- blood glucose
- endoplasmic reticulum stress
- skeletal muscle
- cell cycle arrest
- endothelial cells
- cardiovascular disease
- fatty acid
- uric acid
- weight loss
- physical activity