Serotonin uptake stimulating peptide found in plasma of normal individuals and in some autistic urines

Pedersen, O. S.; Liu, Y.; Reichelt, Karl L.

doi:10.1034/j.1399-3011.1999.00058.x

Cited by 20 publications

(18 citation statements)

References 28 publications

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“…The possible involvement of carboxypeptidases in the pathology of autism is raised by several reports of abnormal patterns of urinary peptides in some individuals with autism. [19][20][21] Although these findings have failed to be replicated by other studies and remain controversial, 22 it is possible that altered pancreatic peptidase function could lead to an unusual accumulation of peptides. Furthermore, the presence of CPA gene transcripts has been identified at low levels in extrapancreatic tissues, namely in brain, where they could potentially participate in signalling events such as biosynthesis or inactivation of peptide messengers.…”

Section: Introductionmentioning

confidence: 48%

Mutation screening and imprinting analysis of four candidate genes for autism in the 7q32 region

Bonora

Bacchelli

et al. 2002

Mol Psychiatry

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Genetic studies indicate that chromosome 7q is likely to contain an autism susceptibility locus (AUTS1). We have followed a positional candidate gene approach to identify the relevant gene and report the analysis of four adjacent genes localised to a 800 kb region in 7q32 that contains an imprinted domain: PEG1/MEST, COPG2, CPA1 and CPA5-a previously uncharacterised member of the carboxypeptidase gene family. Screening these genes for DNA changes and association analysis using intragenic single nucleotide polymorphisms (SNPs) provided no evidence for an etiological role in IMGSAC families. We also searched for imprinting mutations potentially implicated in autism: analysis of both DNA methylation and replication timing indicated a normal imprinting regulation of the PEG1/COPG2 domain in blood lymphocytes of all patients tested. The analysis of these four genes strongly suggests that they do not play a major role in autism aetiology, and delineates our strategy to screen additional candidate genes in the AUTS1 locus.

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Section: Introductionmentioning

confidence: 48%

Mutation screening and imprinting analysis of four candidate genes for autism in the 7q32 region

Bonora

Bacchelli

et al. 2002

Mol Psychiatry

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“…2 This finding was considered inconsistent with reports of low serum levels of serotonin, until the discovery that platelet serotonin levels were also high for autistic children. 19 Pedersen et al 20 have since identified opioid peptide fragments within the urine of autistic children that stimulate serotonin uptake by platelets. It seems possible that, with a high uptake of serotonin by platelets, an increase in serotonin synthesis might result, depleting levels of tryptophan and causing a reduction in urinary levels.…”

Section: Discussionmentioning

confidence: 99%

Altered amino acid excretion in children with autism

Evans

Dunstan

Rothkirch

et al. 2008

Nutritional Neuroscience

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Autism is a complex and life-long behavioural disorder of unknown aetiology. Recent reports have indicated the involvement of digestive tract dysfunction and possible complications from inadequate nutrition. In this study, 34 autistic children (12 untreated and 22 receiving therapeutic treatments related to digestive function and nutritional uptake) and 29 control subjects (all 5-15 years of age) were investigated to determine whether there were any anomalies in the urinary excretion of amino acids, glucose, sucrose, arabinose and tartaric acid using GC/FID and GC/MS analysis techniques. Significantly lower relative urinary levels of essential amino acids were revealed for both the untreated (mean +/- SEM, 32.53 +/- 3.09%) and treated (31.98 +/- 2.87%) autistic children compared with the controls (37.87 +/- 1.50%). There were no significant differences in measured excretions of sugars or tartaric acid. It was concluded that the untreated autistic children had evidence of altered metabolic homeostasis.

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“…A chemical candidate for this reactive inhibition and habituation is serotonin. We found a peptide from autistic urines (pyroGlu-Trp-GlyNH2) that increased the uptake of serotonin into platelets (Pedersen et al, 1999) and into synapses in the CNS (Persico et al, 1998). Increased platelet serotonin is a frequently reported finding in autism (Rogeness et al, 1992).…”

Section: Poor Habituationmentioning

confidence: 96%

Can the Pathophysiology of Autism be Explained by the Nature of the Discovered Urine Peptides?

Reichelt¹,

Knivsberg

2003

Nutritional Neuroscience

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Opioid peptides derived from food proteins (exorphins) have been found in urine of autistic patients. Based on the work of several groups, we try to show that exorphins and serotonin uptake stimulating factors may explain many of the signs and symptoms seen in autistic disorders. The individual symptoms ought to be explainable by the properties and behavioural effects of the found peptides. The data presented form the basis of an autism model, where we suggest that exorphins and serotonin uptake modulators are key mediators for the development of autism. This may be due to a genetically based peptidase deficiency in at least two or more peptidases and, or of peptidase regulating proteins made manifest by a dietary overload of exorphin precursors such as by increased gut uptake.

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Serotonin uptake stimulating peptide found in plasma of normal individuals and in some autistic urines

Cited by 20 publications

References 28 publications

Mutation screening and imprinting analysis of four candidate genes for autism in the 7q32 region

Mutation screening and imprinting analysis of four candidate genes for autism in the 7q32 region

Altered amino acid excretion in children with autism

Can the Pathophysiology of Autism be Explained by the Nature of the Discovered Urine Peptides?

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