Metabolic Signatures of Pediatric Endocrine and Metabolic Disorders

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: 20 July 2026 | Viewed by 446

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Department of Nursing Sciences, Physiotherapy, and Medicine, Faculty of Health Sciences, University of Almería, 04120 Almería, Spain
Interests: pediatric diabetes and endocrinology
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Special Issue Information

Dear Colleagues,

Pediatric endocrine and metabolic disorders, such as obesity; type 1, type 2, and monogenic diabetes; MASLD/MASH (Metabolic Dysfunction-Associated Steatotic Liver Disease and Metabolic Dysfunction-Associated Steatohepatitis); thyroid dysfunction; and disorders of growth and puberty, are characterized by complex metabolic disturbances that often begin long before overt clinical manifestations. Recent advances in metabolomics, metabolic pathway analysis, and multi-omics integration offer new opportunities to identify early metabolic changes, define disease phenotypes, and explore interactions between genetic, hormonal, nutritional, and environmental factors in childhood.

This Special Issue aims to bring together original research and reviews that investigate metabolite profiles, metabolic pathways, and metabolic perturbations across the pediatric endocrine spectrum. We welcome studies analyzing alterations in metabolites; environmental or dietary influences on metabolism; metabolic biomarkers for risk stratification; and methodological or technological innovations that enhance understanding of pediatric metabolic diseases. Submissions integrating metabolomics with clinical phenotyping, longitudinal designs, or systems biology approaches are especially encouraged.

Dr. Tiago Jeronimo dos Santos
Guest Editor

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Keywords

  • pediatric metabolomics
  • endocrine disorders
  • type 1 diabetes
  • type 2 diabetes
  • childhood obesity
  • insulin resistance
  • metabolic pathways
  • MASLD/MASH
  • biomarkers
  • environmental metabolic perturbations
  • multi-omics

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Published Papers (1 paper)

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Research

28 pages, 3503 KB  
Article
A Multi-Omics Approach Uncovers Divergent Mechanisms of Asthma in Normal Weight and Obese Children
by Ilhame Diboun, Harshita Shailesh, Shana Jacob, Mohamed A. Elrayess, Stefan Worgall, Younes Mokrab and Ibrahim Janahi
Metabolites 2026, 16(5), 333; https://doi.org/10.3390/metabo16050333 - 15 May 2026
Viewed by 216
Abstract
Background: Children with obesity-related asthma exhibit poorer symptom control and more frequent exacerbations than their normal-weight peers, but the underlying metabolic mechanisms are unclear. This study aimed to identify drivers of obesity-related asthma through untargeted plasma metabolomic and lipidomic profiling. Methods: [...] Read more.
Background: Children with obesity-related asthma exhibit poorer symptom control and more frequent exacerbations than their normal-weight peers, but the underlying metabolic mechanisms are unclear. This study aimed to identify drivers of obesity-related asthma through untargeted plasma metabolomic and lipidomic profiling. Methods: Plasma was obtained from normal weight (NW) asthmatic (n = 95) and non-asthmatic (n = 67) and overweight/obese (OO) asthmatic (n = 99) and non-asthmatic (n = 100) children (6–17 years). We assessed metabolic and lipidomic differences between asthmatics and controls within each BMI group using orthogonal partial least squares discriminant analysis (OPLS-DA), examined overlap with the adult Qatar Biobank cohort, and mapped metabolic–clinical interactions using Gaussian Graphical Models. Results: In the fitted OPLS-DA models, separation between asthmatic and control groups was stronger in the NW group (R2Y = 0.72/0.52) than in OO (R2Y = 0.65/0.63) children. Asthma was associated with altered tricarboxylic acid (TCA) intermediates, ether-linked phosphatidylethanolamines, and sphingomyelins (SM) in NW, and with phosphatidylcholines, lysophosphatidylcholines, and phosphatidylethanolamines in OO. Integrating metabolomic, lipidomic, and clinical data revealed connections between altered SMs and interleukins, and TCA intermediates and electrolytes, all associated with elevated leptin in NW. An increased residual volume to total lung capacity ratio in OO was associated with phospholipid shifts. The overall dynamics in lipid metabolism with asthma, conditioned on BMI, was also observed in the adult Qatar Biobank cohort. Conclusions: Among NW children with asthma, we found enhanced TCA cycle activity and inflammation linked to altered SM metabolism, whereas in OO, the findings suggest oxidative stress arising from chronic obesity-related inflammation. These data reveal BMI-specific metabolic mechanisms of pediatric asthma that might inform precision approaches to disease management. Full article
(This article belongs to the Special Issue Metabolic Signatures of Pediatric Endocrine and Metabolic Disorders)
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