[article]
| Titre : |
Disrupted fetal carbohydrate metabolism in children with autism spectrum disorder |
| Type de document : |
texte imprimé |
| Auteurs : |
Serena B. GUMUSOGLU, Auteur ; Brandon M. SCHICKLING, Auteur ; Donna A. SANTILLAN, Auteur ; Lynn M. TEESCH, Auteur ; Mark K. SANTILLAN, Auteur |
| Langues : |
Anglais (eng) |
| Mots-clés : |
Humans Autism Spectrum Disorder/metabolism/blood/diagnosis Female Male Carbohydrate Metabolism/physiology Biomarkers/blood Fetal Blood/metabolism Metabolomics Child Pregnancy Gas Chromatography-Mass Spectrometry Case-Control Studies Autism Carbohydrates Cord blood Monosaccharides Polysaccharides used in this study are derived from a tissue bank which is approved by the University of Iowa Institutional Review Board (IRB #: 200910784). This study was performed in line with the principles of the Declaration of Helsinki. Informed consent was obtained from all individual participants included in the study. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests. |
| Index. décimale : |
PER Périodiques |
| Résumé : |
BACKGROUND: Despite the power and promise of early detection and treatment in autism spectrum disorder (ASD), early-life biomarkers are limited. An early-life risk biosignature would advance the field's understanding of ASD pathogenies and targets for early diagnosis and intervention. We therefore sought to add to the growing ASD biomarker literature and evaluate whether fetal metabolomics are altered in idiopathic ASD. METHODS: Banked cord blood plasma samples (N = 36 control, 16 ASD) were analyzed via gas chromatography and mass spectrometry (GC-MS). Samples were from babies later diagnosed with idiopathic ASD (non-familial, non-syndromic) or matched, neurotypical controls. Metabolite set enrichment analysis (MSEA) and biomarker prediction were performed (MetaboAnalyst). RESULTS: We detected 76 metabolites in all samples. Of these, 20 metabolites differed significantly between groups: 10 increased and 10 decreased in ASD samples relative to neurotypical controls (p < 0.05). MSEA revealed significant changes in metabolic pathways related to carbohydrate metabolism and glycemic control. Untargeted principle components analysis of all metabolites did not reveal group differences, while targeted biomarker assessment (using only Fructose 6-phosphate, D-Mannose, and D-Fructose) by a Random Forest algorithm generated an area under the curve (AUC) = 0.766 (95% CI: 0.612-0.896) for ASD prediction. CONCLUSIONS: Despite a high and increasing prevalence, ASD has no definitive biomarkers or available treatments for its core symptoms. ASD's earliest developmental antecedents remain unclear. We find that fetal plasma metabolomics differ with child ASD status, in particular invoking altered carbohydrate metabolism. While prior clinical and preclinical work has linked carbohydrate metabolism to ASD, no prior fetal studies have reported these disruptions in neonates or fetuses who go on to be diagnosed with ASD. Future work will investigate concordance with maternal metabolomics to determine maternal-fetal mechanisms. |
| En ligne : |
https://dx.doi.org/10.1186/s11689-025-09601-z |
| Permalink : |
https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 |
in Journal of Neurodevelopmental Disorders > 17 (2025)
[article] Disrupted fetal carbohydrate metabolism in children with autism spectrum disorder [texte imprimé] / Serena B. GUMUSOGLU, Auteur ; Brandon M. SCHICKLING, Auteur ; Donna A. SANTILLAN, Auteur ; Lynn M. TEESCH, Auteur ; Mark K. SANTILLAN, Auteur. Langues : Anglais ( eng) in Journal of Neurodevelopmental Disorders > 17 (2025)
| Mots-clés : |
Humans Autism Spectrum Disorder/metabolism/blood/diagnosis Female Male Carbohydrate Metabolism/physiology Biomarkers/blood Fetal Blood/metabolism Metabolomics Child Pregnancy Gas Chromatography-Mass Spectrometry Case-Control Studies Autism Carbohydrates Cord blood Monosaccharides Polysaccharides used in this study are derived from a tissue bank which is approved by the University of Iowa Institutional Review Board (IRB #: 200910784). This study was performed in line with the principles of the Declaration of Helsinki. Informed consent was obtained from all individual participants included in the study. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests. |
| Index. décimale : |
PER Périodiques |
| Résumé : |
BACKGROUND: Despite the power and promise of early detection and treatment in autism spectrum disorder (ASD), early-life biomarkers are limited. An early-life risk biosignature would advance the field's understanding of ASD pathogenies and targets for early diagnosis and intervention. We therefore sought to add to the growing ASD biomarker literature and evaluate whether fetal metabolomics are altered in idiopathic ASD. METHODS: Banked cord blood plasma samples (N = 36 control, 16 ASD) were analyzed via gas chromatography and mass spectrometry (GC-MS). Samples were from babies later diagnosed with idiopathic ASD (non-familial, non-syndromic) or matched, neurotypical controls. Metabolite set enrichment analysis (MSEA) and biomarker prediction were performed (MetaboAnalyst). RESULTS: We detected 76 metabolites in all samples. Of these, 20 metabolites differed significantly between groups: 10 increased and 10 decreased in ASD samples relative to neurotypical controls (p < 0.05). MSEA revealed significant changes in metabolic pathways related to carbohydrate metabolism and glycemic control. Untargeted principle components analysis of all metabolites did not reveal group differences, while targeted biomarker assessment (using only Fructose 6-phosphate, D-Mannose, and D-Fructose) by a Random Forest algorithm generated an area under the curve (AUC) = 0.766 (95% CI: 0.612-0.896) for ASD prediction. CONCLUSIONS: Despite a high and increasing prevalence, ASD has no definitive biomarkers or available treatments for its core symptoms. ASD's earliest developmental antecedents remain unclear. We find that fetal plasma metabolomics differ with child ASD status, in particular invoking altered carbohydrate metabolism. While prior clinical and preclinical work has linked carbohydrate metabolism to ASD, no prior fetal studies have reported these disruptions in neonates or fetuses who go on to be diagnosed with ASD. Future work will investigate concordance with maternal metabolomics to determine maternal-fetal mechanisms. |
| En ligne : |
https://dx.doi.org/10.1186/s11689-025-09601-z |
| Permalink : |
https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 |
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