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Related Concept Videos

Hyperglycemia01:29

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...
Proteoglycans01:05

Proteoglycans

Glycans, a class of complex heterogeneous molecules, can be covalently attached to proteins to form glycosylated proteins that regulate various physiological and pathological processes. Glycosylated proteins or glycoproteins comprise N-linked and O-linked oligosaccharides. O-glycosylation is the most common type of protein glycosylation. Here, glycans attach to the oxygen atom of the hydroxyl groups of Serine or Threonine residues. O-linked glycosylation occurs later in protein processing,...
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...
Protein Glycosylation01:25

Protein Glycosylation

Glycosylation, the most common post-translational modification for proteins, serves diverse functions. Adding sugars to proteins makes the proteins more resistant to proteolytic digestion. Glycosylated proteins can act as markers and receptors to promote cell-cell adhesion. Additionally, they have many essential quality control functions in the cell, such as correct protein folding and facilitating transport of misfolded proteins to the cytosol, which can be degraded.
Glycosylation occurs in...
Oligosaccharide Assembly01:24

Oligosaccharide Assembly

Protein glycosylation starts in the ER lumen and continues in the Golgi apparatus. Glycosyltransferases catalyze the addition of sugar molecules or glycosylation of proteins. Usually, these enzymes add sugars to the hydroxyl groups of selected serine or threonine residues to form O-linked glycans or the amino groups of asparagine residues to form N-linked glycans. Different positions on the same polypeptide chain can contain differently linked glycans.
Multiple sugar molecules that may or may...
Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...

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Related Experiment Video

Updated: Jun 13, 2026

Analyzing the Permeability of the Blood-Brain Barrier by Microbial Traversal through Microvascular Endothelial Cells
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Analyzing the Permeability of the Blood-Brain Barrier by Microbial Traversal through Microvascular Endothelial Cells

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[Glycation].

Sho-ichi Yamagishi1

  • 1Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine.

Nihon Rinsho. Japanese Journal of Clinical Medicine
|May 8, 2010
PubMed
Summary

Diabetic cardiovascular disease (CVD) risk is reduced by intensive therapy due to

Area of Science:

  • Endocrinology and Metabolism
  • Cardiovascular Research
  • Diabetology

Background:

  • Metabolic memory influences cardiovascular disease (CVD) pathogenesis in diabetes.
  • Intensive therapy in the Diabetes Control and Complications Trial (DCCT) reduced CVD events by 50% in type 1 diabetes patients years later.
  • Advanced glycation end products (AGEs) accumulation is a key mechanism of metabolic memory in diabetes.

Purpose of the Study:

  • To review the role of the AGE-RAGE axis in diabetic macroangiopathy.
  • To explore AGEs and their receptor RAGE interaction in CVD in diabetes.
  • To highlight the AGE-RAGE system as a potential therapeutic target for diabetic CVD.

Main Methods:

  • Literature review of clinical studies and biochemical pathways.

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Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish

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Analyzing the Permeability of the Blood-Brain Barrier by Microbial Traversal through Microvascular Endothelial Cells
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  • Analysis of data from DCCT-EDIC Research on metabolic memory and CVD.
  • Examination of the AGE-RAGE interaction in the context of diabetic macroangiopathy.

    • Main Results:

    • Metabolic memory is substantiated by clinical studies in diabetic CVD.
    • AGEs formation and accumulation align with the metabolic memory theory.
    • AGE-RAGE axis interaction is implicated in CVD development in diabetes.

    Conclusions:

    • The AGE-RAGE system is a significant factor in diabetic macroangiopathy.
    • Blocking the AGE-RAGE interaction presents a promising therapeutic strategy for diabetic CVD.
    • Understanding metabolic memory mechanisms, particularly AGEs, is crucial for managing diabetic complications.