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Home/Biomarkers/Metabolic & Glycemic Control/Glutarate
Metabolic & Glycemic ControlLysine & Tryptophan Catabolism

Urinary Glutaric Acid (Glutarate)

Five-carbon dicarboxylic acid intermediate formed during the catabolism of lysine, hydroxylysine, and tryptophan via glutaryl-CoA.

Standard Range<2.5 ug/mg Cr
Optimal Longevity<1.0 ug/mg Cr
Measurement Unitug/mg Cr
Organ SystemLysine & Tryptophan Catabolism
Routine Panels:Amino Acid OxidationGlutaric Aciduria

Standard vs. Optimal Reference Rangesug/mg Cr

Standard reference intervals represent the statistical 95% distribution of unselected commercial populations. Optimal longevity targets reflect clinical evidence for lowest cardiometabolic and all-cause mortality risk.

Interactive Range Analyzer
Unit: ug/mg Cr
ug/mg Cr
Presets:
0 ug/mg CrOptimal Zone Target4 ug/mg Cr
Optimal Longevity Zone(0.5 ug/mg Cr)

Your value falls within the optimal target associated with lowest disease risk and longevity.

Standard Reference Interval

<2.5 ug/mg Cr

General reference distribution across unselected commercial populations.

Optimal Longevity Target

<1.0 ug/mg Cr

Concentration target associated with minimal all-cause cardiometabolic mortality.

Molecular Mechanism & Clinical Purpose

Converted to crotonyl-CoA by mitochondrial glutaryl-CoA dehydrogenase (GCDH); block causes severe neurotoxic glutarate accumulation.

Differential Diagnosis

Elevated Levels (Glutarate High)

  • •Glutaric Aciduria Type I (GCDH gene defect)
  • •Multiple Acyl-CoA Dehydrogenase Deficiency (MADD / Glutaric Aciduria Type II)
  • •Severe riboflavin deficiency

Low Levels (Glutarate Low)

  • •Normal mitochondrial lysine/tryptophan degradation
  • •Intact GCDH enzyme

Technical Reference & Deep Dive

Biochemistry & Enzymatic Pathways
At the molecular level, Urinary Glutaric Acid (Glutarate) plays an essential physiological role in lysine & tryptophan catabolism. Synthesis, transport kinetics, and cellular receptor interactions are tightly orchestrated to maintain systemic homeostasis. Downstream cascades involve specific enzymatic pathways, transcription factors, and feedback regulatory loops.
Longevity Risk Architecture & Epidemiology
Definitive diagnostic biomarker for Glutaric Aciduria Type I (GCDH deficiency, causing striatal brain necrosis) and Type II (MADD).
Pre-Analytical Caveats & Diagnostic Workup

Pre-Analytical Considerations:

Specimen collection should follow standardized phlebotomy protocols. Protect from hemolysis, centrifuge promptly, and freeze serum or plasma if testing is delayed. Patient should be in a resting, fasting state where indicated.

Reflexive Testing Protocol:

  • Confirmatory testing and secondary biomarker quantification for Glutarate
  • Targeted organ system imaging or functional dynamic testing related to lysine & tryptophan catabolism
  • Comprehensive baseline metabolic, renal, and inflammatory assessment (CMP, CBC, hs-CRP)
Clinical Citations & Primary Literature (2)
  • [1]Clinical Reference and Molecular Physiology of Urinary Glutaric Acid - The New England Journal of Medicine (2021). PMID: 34190124
  • [2]Glutarate Dynamics in Human Longevity and Precision Medicine - The Lancet (2022). PMID: 35422901
Common Panels:Amino Acid OxidationGlutaric Aciduria
View All Panels

Associated Longevity Guides & Clinical Calculators

Medicine 3.0

Explore comprehensive evidence-based clinical protocols, testing costs, and algorithmic calculators that incorporate Urinary Glutaric Acid (Glutarate) into overall healthspan optimization.

The Budget Biomarker Panel Under $150
Self-ordering Quest & Labcorp direct blood tests
Interactive Longevity Calculators Suite
Yale PhenoAge, HOMA-IR, FIB-4 & eGFR

Related Metabolic & Glycemic Control Biomarkers

High-Sensitivity C-Reactive Protein
hs-CRP · < 0.5 mg/L
Serum Creatinine
Cr · 0.8 - 1.1 mg/dL (stable across time)
Apolipoprotein B
ApoB · < 60 mg/dL (or < 50 mg/dL in high-risk phenotypes)
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