Mujeeb Afeefa Parveen

Moldova

Glycated end products and the effect of chronic hyperglycaemia on liver function

Afeefa parveen mujeeb 1, Anaswara Vijayakumar kuzhipurayidathil 1, Turcanu Adela 2
1. Nicolae testimitanu state university of medicine and pharmacy, chisinau , Moldova
2. University lecturer, department of gastroenterology – Nicolae testimitanu state university of medicine and pharmacy, chisinau , Moldova

Abstract

Background

Complex compounds known as glycated end products (AGEs) are created when reducing sugars and amino groups on proteins lipids or nucleic acids interact non-enzymatically. This process known as glycation is frequently made worse by persistent hyperglycemia which is a hallmark of uncontrolled diabetes mellitus. AGEs have been linked to a number of clinical disorders due to their capacity to induce tissue damage inflammation and oxidative stress. The liver is particularly vulnerable to the harmful effects of AGEs because of its function in glucose metabolism and detoxification. AGE buildup in the liver has been specifically linked to progressive liver diseases like cirrhosis fibrosis and hepatic steatosis.

Methods

The bibliographic sources included in the study were based on online resources published between 2014 and 2024, including PubMed, Google Scholar, Science Direct, and others.

Results

Oxidative stress inflammation and fibrosis are brought on by AGE accumulation which is especially common in the liver an organ important for glucose metabolism and detoxification. Hepatocytes express the receptor for advanced glycation end products (RAGE) which when activated causes oxidative damage and reactive oxygen species (ROS). The activation of hepatic stellate cells by AGE-induced RAGE signaling results in the deposition of extracellular matrix components particularly collagen which causes fibrosis. Fibrosis is exacerbated by an imbalance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). AGE accumulation has been linked to increased liver enzymes and histological indicators like fibrosis lipid infiltration and hepatocyte degeneration according to research.

Conclusions

Hepatocellular injury liver scarring and collagen deposition are all significantly influenced by the AGE-RAGE signaling pathway. Because of these changes patients with diabetes often have decreased liver function. Notwithstanding promising preclinical studies on AGE inhibitors and antioxidants as potential treatment modalities clinical translation has been subpar. More study is needed to better understand the processes driving AGE-mediated liver damage and establish more effective treatment approaches in diabetics. Reducing hyperglycemia and treating the AGE-RAGE line may assist persons with the syndrome achieve better long-term outcomes and fewer liver damage.