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Functional Assessment of Urinary Neuro-biogenic Amines—A COMPREHENSIVE GUIDE 


tem. Deficient function of the serotonin

transporter (SERT) may prevent normal

reuptake of serotonin by pre-synaptic

neurons, and result in elevated sero-

tonin and 5-HIAA levels. Platelets take

up 10% of plasma serotonin. The sero-

tonin released when platelets aggregate

may contribute to vasoconstriction and

the symptoms of metabolic syndrome in

some populations. During the “first pass”

through hepatic circulation, the liver

metabolizes 30-80% of GI serotonin to

5-hydroxyindoleacetic acid (5-HIAA).

Serotonin may also be converted to

5-HIAA in the lungs. Serotonin is con-

verted into melatonin by the enzyme

arylalkylamine N-acetyltransferase; defi-

cient function of this enzyme may result

in elevated serotonin and 5-HIAA levels

and low melatonin levels.


5-HIAA is not known to bind with

neurotransmitter receptors.


MAO-A SNPs (DNA Methylation



American Association for Clinical Chemistry

Accessed 19 December 2014

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Hitoshi; Asano, Mai; Yamazaki, Masahiro

et al. (2012)

High plasma 5-hydroxyindole-3-acetic acid

concentrations in subjects with metabolic


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Association Between Urinary Albumin

Excretion and Plasma 5-Hydroxyindole-

3-Acetic Acid Concentration in Men

With Type 2 Diabetes

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5-hydroxyindole acetic acid (5-HIAA) cle/2089202-overview

retreived 02 Sept


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Serotonin and GI Disorders: An Update on

Clinical and Experimental Studies

American College of Gastroenterology

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p. e13

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Dzurik R (2001)

Serotonin and 5-hydroxyindole-acetic acid

Bratisl Lek Listy 2001; 102 (8): 351.356

Spiller, R (2007)

Recent advances in understanding the role

of serotonin in gastrointestinal motility

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Neurogastroenterology and motility : the official

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Tryptamine is derived from the essen-

tial amino acid tryptophan. Tryptamine

and other “trace amines” are found at

very low (nanmolar) levels in nerve cells.

The interaction of trace amines, and their

receptors, in the brain may play a role in

psychiatric and neurological disease pro-

cesses. Experimental evidence suggests

that dysregulation of trace amines may

alter levels of dopamine, norepinephrine

or serotonin, and thereby contribute to

neuropsychiatric disorders such as at-

tention deficit hyperactivity disorder

(ADHD), schizophrenia, depression and

neurodegenerative diseases. Tryptamine