ArticleiScience2023
Cord serum metabolic signatures of future progression to immune-mediated diseases.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Epigenetic analyses suggest different pathways during pregnancy for development of type 1 diabetes in children with high versus low-neutral human leukocyte antigen-risk.Journal of internal medicine · 2026Article
- The inflammatory path toward type 1 diabetes begins during pregnancy.Nature communications · 2026Article
- Epigenetic-proteomic network crosstalk at birth across HLA risk groups in type 1 diabetes.Frontiers in immunology · 2026Article
- Prenatal exposure to environmental contaminants and cord serum metabolite profiles in future immune-mediated diseases.Journal of exposure science & environmental epidemiology · 2024Article
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous prospective studies suggest that progression to autoimmune diseases is preceded by metabolic dysregulation, but it is not clear which metabolic changes are disease-specific and which are common across multiple immune-mediated diseases. Here we investigated metabolic profiles in cord serum in a general population cohort (All Babies In Southeast Sweden; ABIS), comprising infants who progressed to one or more immune-mediated diseases later in life: type 1 diabetes (n = 12), celiac disease (n = 28), juvenile idiopathic arthritis (n = 9), inflammatory bowel disease (n = 7), and hypothyroidism (n = 6); and matched controls (n = 270). We observed elevated levels of multiple triacylglycerols (TGs) an alteration in several gut microbiota related metabolites in the autoimmune groups. The most distinct differences were observed in those infants who later developed HT. The specific similarities observed in metabolic profiles across autoimmune diseases suggest that they share specific common metabolic phenotypes at birth that contrast with those of healthy controls.
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Registered trials
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