Related Experiment Video

Updated: May 15, 2026

Improving IV Insulin Administration in a Community Hospital
12:08

Improving IV Insulin Administration in a Community Hospital

Published on: June 11, 2012

Current therapeutic interventions in the glycation pathway: evidence from clinical studies

L Engelen1, C D A Stehouwer, C G Schalkwijk

  • 1Department of Internal Medicine, CARIM School for Cardiovascular Diseases, Maastricht University Medical Centre, Maastricht, The Netherlands.

Diabetes, Obesity & Metabolism
|January 3, 2013
PubMed

Insights

Clinical evidence for interventions targeting advanced glycation endproducts (AGEs) to prevent diabetes complications is currently weak. Specific AGE inhibitors and breakers show safety or efficacy concerns, and B vitamin data is limited.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Vascular Biology

Background:

  • Increased formation of advanced glycation endproducts (AGEs) is linked to diabetic micro- and macrovascular complications.
  • In vitro and animal studies suggest interventions like aminoguanidine, alagebrium, pyridoxamine, thiamine, and benfotiamine can inhibit AGE formation or action.

Purpose of the Study:

  • To review current clinical evidence on interventions targeting the glycation pathway for diabetic vascular disease.
  • To assess the clinical benefits of specific AGE inhibitors and breakers.
  • To evaluate potential AGE-inhibiting effects of therapies not primarily developed for glycation.

Main Methods:

  • Systematic review of clinical studies evaluating AGE inhibitors, AGE breakers, and other therapies with potential AGE-inhibiting effects.
  • Analysis of safety and efficacy data from human trials.
  • Assessment of study designs and measurement techniques for AGE-related therapies.

Main Results:

  • Clinical studies on aminoguanidine (AGE inhibitor) and alagebrium (AGE breaker) raise concerns regarding safety and/or efficacy.
  • Limited clinical evidence exists for the AGE-inhibiting effects of B vitamins (pyridoxamine, thiamine, benfotiamine).
  • Evidence for AGE inhibition by unrelated therapies is hampered by heterogeneous and often sub-optimal study designs and measurement techniques.

Conclusions:

  • Current clinical evidence supporting interventions to inhibit AGE formation or action in diabetes is weak and unconvincing.
  • Further well-designed clinical trials are needed to establish the safety and efficacy of AGE-targeted therapies.
Keywords:
advanced glycation endproductscardiovascular diseasediabetes mellitustherapy

More Related Videos

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory10:03

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory

Published on: February 28, 2013

Related Concept Videos

Diabetes: Management and Pharmacotherapy01:15

Diabetes: Management and Pharmacotherapy

The therapy for diabetes aims to alleviate hyperglycemia-related symptoms, prevent acute metabolic decompensation, and reduce chronic end-organ complications. Glycemic control is evaluated through short-term (self-monitoring, continuous glucose monitoring) and long-term (A1c, fructosamine) metrics, enabling near real-time tracking of blood glucose levels and reflecting glycemic control over specific time frames.
Insulin remains the cornerstone of treatment for most patients with type 1 and many...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Glucose Transporters01:27

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are typically...
Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...