Abstract
Advanced Glycation Endproducts (AGEs) are a group of heterogeneous compounds formed by the non enzymatic reactions between aldehydic group of reducing sugars with proteins, lipids or nucleic acids. Formation and accumulation of AGEs are related with the aging process and are accelerated in diabetes. Type 2 diabetes are the most common form of diabetes, which are characterized by hyperglycemia and insulin resistance associated to a progressive deterioration of beta cell function and mass. The pathogenic role of AGEs in vascular diabetic complications is widely recognised. Recently, other aspects of the detrimental effects of AGEs in type 2 diabetes have emerged: AGEs interfere with the complex molecular pathway of insulin signalling, leading to insulin resistance; AGEs modify the insulin molecule, and consequently, its function; AGEs decrease insulin secretion and insulin content. In this article, we review the role of AGEs in type 2 diabetes, beyond their involvement in vascular complications.
Keywords: Diabetes, advanced glycation end products, pancreatic β-cells, insulin resistance, metabolic syndrome, hyperglycemia, glucose homeostasis, methylglyoxal, glycolaldehyde, AGE pentosidine, phosphorylation, musculoskeletal tissues
Endocrine, Metabolic & Immune Disorders - Drug Targets
Title: Advanced Glycation Endproducts and Diabetes. Beyond Vascular Complications
Volume: 11 Issue: 2
Author(s): Alessandra Puddu and Giorgio L. Viviani
Affiliation:
Keywords: Diabetes, advanced glycation end products, pancreatic β-cells, insulin resistance, metabolic syndrome, hyperglycemia, glucose homeostasis, methylglyoxal, glycolaldehyde, AGE pentosidine, phosphorylation, musculoskeletal tissues
Abstract: Advanced Glycation Endproducts (AGEs) are a group of heterogeneous compounds formed by the non enzymatic reactions between aldehydic group of reducing sugars with proteins, lipids or nucleic acids. Formation and accumulation of AGEs are related with the aging process and are accelerated in diabetes. Type 2 diabetes are the most common form of diabetes, which are characterized by hyperglycemia and insulin resistance associated to a progressive deterioration of beta cell function and mass. The pathogenic role of AGEs in vascular diabetic complications is widely recognised. Recently, other aspects of the detrimental effects of AGEs in type 2 diabetes have emerged: AGEs interfere with the complex molecular pathway of insulin signalling, leading to insulin resistance; AGEs modify the insulin molecule, and consequently, its function; AGEs decrease insulin secretion and insulin content. In this article, we review the role of AGEs in type 2 diabetes, beyond their involvement in vascular complications.
Export Options
About this article
Cite this article as:
Puddu Alessandra and L. Viviani Giorgio, Advanced Glycation Endproducts and Diabetes. Beyond Vascular Complications, Endocrine, Metabolic & Immune Disorders - Drug Targets 2011; 11 (2) . https://dx.doi.org/10.2174/187153011795564115
DOI https://dx.doi.org/10.2174/187153011795564115 |
Print ISSN 1871-5303 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3873 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Flow Cytometry Study of Leukocyte Function: Analytical Comparison of Methods and their Applicability to Clinical Research
Current Medicinal Chemistry Effect of Diabetes on The Blood Brain Barrier
Current Pharmaceutical Design Astrocytes: New Targets for the Treatment of Neurodegenerative Diseases
Current Pharmaceutical Design Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) and Other Anti- Inflammatory Agents in the Treatment of Neurodegenerative Disease
Current Alzheimer Research Effects of Vitamin C and E Against Oxidative Stress: Is Antioxidant Supplementation Efficient?
Current Nutraceuticals Metabotropic Purinergic Receptors in Lipid Membrane Microdomains
Current Medicinal Chemistry Crossed Cerebellar Diaschisis in Alzheimer’s Disease
Current Alzheimer Research CCL2-CCR2 Signaling in Disease Pathogenesis
Endocrine, Metabolic & Immune Disorders - Drug Targets Potential for Treatment of Neurodegenerative Diseases with Natural Products or Synthetic Compounds that Stabilize Microtubules
Current Pharmaceutical Design P2X Receptors and Diabetes
Current Medicinal Chemistry Oxidative Stress in the Pathogenesis/Treatment of Diabetes and its Complications
Current Nutrition & Food Science Oxidative Stress and Mitochondrial Impairment After Treatment with Anti-HIV Drugs: Clinical Implications
Current Pharmaceutical Design Assessing Glutamatergic Function and Dysfunction in Peripheral Tissues
Current Medicinal Chemistry Neurobiology of Sleep Disturbances in Neurodegenerative Disorders
Current Pharmaceutical Design TNF α Signaling Beholds Thalidomide Saga: A Review of Mechanistic Role of TNF-α Signaling Under Thalidomide
Current Topics in Medicinal Chemistry Structures Required of Flavonoids for Inhibiting Digestive Enzymes
Anti-Cancer Agents in Medicinal Chemistry Study of Irisin Hormone Level in Type 2 Diabetic Patients and Patients with Diabetic Nephropathy
Current Diabetes Reviews The Chaperone-like Activity of Rat HspB8/Hsp22 and Dynamic Molecular Transition Related to Oligomeric Architectures In Vitro
Protein & Peptide Letters GEMSP: A New Therapeutic Approach to Multiple Sclerosis
Central Nervous System Agents in Medicinal Chemistry Proteomics Annotation of Lipid Rafts Modified by Virus Infection
Combinatorial Chemistry & High Throughput Screening