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Related Concept Videos

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...
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,...
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...
Glycosaminoglycans01:23

Glycosaminoglycans

Glycosaminoglycans (GAGs), also known as mucopolysaccharides, are long and linear polymers comprising of specific repeating disaccharides - the amino sugar that can be N-acetylglucosamine or N-acetylgalactosamine, and a uronic acid that is usually glucuronic acid or iduronic acid.
GAGS are found in the extracellular matrix of vertebrates, invertebrates, and bacteria. Due to their polar nature they attract water, and serve as excellent lubricants or shock absorbers in an animal body.
Hyaluronic...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...

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Related Experiment Video

Updated: Jun 1, 2026

Advanced Glycation End-Products Sensitize Human Sensory-Like Neuron Cells to Capsaicin-Induced Calcium Influx
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Published on: May 2, 2025

Advanced glycation end products.

Merlin C Thomas1

  • 1Baker IDI Heart and Diabetes Institute, Melbourne, Vic., Australia.

Contributions to Nephrology
|June 11, 2011
PubMed
Summary
This summary is machine-generated.

Advanced glycation end products (AGEs) contribute to diabetic kidney disease by damaging kidney proteins and promoting inflammation. Inhibiting AGEs shows promise in slowing disease progression, though clinical effectiveness is still under investigation.

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Area of Science:

  • Nephrology
  • Endocrinology
  • Biochemistry

Background:

  • Diabetes causes hyperglycemia, dyslipidemia, and oxidative stress, leading to advanced glycation end product (AGE) accumulation in the kidneys.
  • AGEs modify kidney proteins and activate receptors, promoting inflammation and fibrosis characteristic of diabetic nephropathy.
  • AGEs synergize with other pathogenic factors like oxidative stress and the renin-angiotensin system, creating a cycle of kidney disease progression.

Purpose of the Study:

  • To investigate the role of AGEs in the pathogenesis of diabetic nephropathy.
  • To explore the potential of AGE inhibitors in mitigating kidney damage associated with diabetes.
  • To understand the balance between AGEs, their receptors, and natural defense mechanisms in diabetic kidney disease.

Main Methods:

  • Review of studies investigating AGE formation, modification of protein targets, and receptor activation in diabetic kidneys.
  • Analysis of research utilizing AGE inhibitors to assess their impact on kidney disease progression in diabetes models.
  • Examination of data on natural AGE defense mechanisms and the expression of AGE receptors in diabetic nephropathy.

Main Results:

  • AGE accumulation and receptor activation are key drivers of renal damage, fibrosis, and inflammation in diabetic nephropathy.
  • Inhibiting AGE formation effectively retards kidney disease development in experimental models, independent of glycemic control.
  • Natural AGE defenses are diminished in diabetic individuals, particularly those with nephropathy, while AGE receptors increase.

Conclusions:

  • AGEs are significant downstream mediators of hyperglycemia-induced kidney damage in diabetes.
  • Pharmacological strategies targeting AGEs have shown efficacy in preclinical models for preventing diabetic kidney disease.
  • Further clinical studies are needed to validate the therapeutic utility of AGE-lowering agents in patients.