Related Experiment Video
Updated: Nov 4, 2025

Preparation of Naringenin Solution for In Vivo Application
Published on: August 10, 2021
Novel advances in inhibiting advanced glycation end product formation using natural compounds
Qinghe Song1, Junjun Liu1, Liyuan Dong1
1Endocrine and Metabolic Diseases Hospital of Shandong First Medical University, Shandong First Medical University & Shandong Academy of Medical Sciences, 18877, Jingshi Rd., Jinan 250001, China.
Abstract:
Advanced glycation end products (AGEs) are a group of complex compounds generated by nonenzymatic interactions between proteins and reducing sugars or lipids. AGEs accumulate in vivo and activate various signaling pathways closely related to the occurrence of various chronic metabolic diseases. In this paper, we describe the process through which AGEs are formed, the classification of AGEs, and biological effects of AGEs on human health. Most importantly, we review recent progress in natural compound-based AGE formation inhibitors. Major classes of natural inhibitors, including polyphenols, polysaccharides, terpenoids, vitamins and alkaloids, have been described. Their mechanisms of action have been summarized as scavenging free radicals, chelating metal ions, capturing active carbonyl compounds, protecting protein glycation sites, and lowering blood glucose levels. Although these natural compounds have good antiglycation activity, to date, they are not widely used in the clinic, likely because of their low content levels. However, these natural compounds and their molecular frameworks will play a valuable role in inspiring drug discovery.
Insights
Advanced glycation end products (AGEs) contribute to chronic diseases. Natural compounds show promise in inhibiting AGE formation through various mechanisms, potentially inspiring new drug discovery.
Area of Science:
- Biochemistry
- Molecular Biology
- Metabolic Diseases
Background:
- Advanced glycation end products (AGEs) are formed via nonenzymatic reactions between proteins/lipids and sugars.
- AGE accumulation in vivo is linked to the pathogenesis of chronic metabolic diseases.
- Understanding AGE formation and biological impact is crucial for disease management.
Purpose of the Study:
- To elucidate the formation, classification, and biological effects of AGEs.
- To review natural compounds that inhibit AGE formation.
- To explore the therapeutic potential of natural antiglycation agents.
Main Methods:
- Literature review of AGE formation pathways and biological effects.
- Compilation and analysis of studies on natural AGE inhibitors.
- Summary of mechanisms of action for natural antiglycation compounds.
Main Results:
- AGEs are implicated in various chronic metabolic diseases.
- Polyphenols, polysaccharides, terpenoids, vitamins, and alkaloids exhibit AGE inhibitory properties.
- Mechanisms include free radical scavenging, metal chelation, and carbonyl trapping.
Conclusions:
- Natural compounds possess significant antiglycation activity.
- Low natural abundance limits current clinical use but highlights potential for drug discovery.
- Natural compound frameworks offer valuable leads for developing novel therapeutic strategies against AGE-related diseases.
More Related Videos
05:08Plate-based Large-scale Cultivation of Caenorhabditis elegans: Sample Preparation for the Study of Metabolic Alterations in Diabetes
Published on: August 24, 2018
09:31Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
Published on: November 5, 2016
Related Concept Videos
Dipeptidyl Peptidase 4 Inhibitors
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors
Acarbose and miglitol are...
Glucagon-like Receptor Agonists
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
Oral Hypoglycemic Agents: Glinides
Oral Hypoglycemic Agents: Biguanides and Glitazones
Enzyme Inhibition