Cord serum lipidome in prediction of islet autoimmunity and type 1 diabetes

Matej Orešič (Corresponding Author), Peddinti Gopalacharyulu, Juha Mykkänen, Niina Lietzen, Marjaana Mäkinen, Heli Nygren, Satu Simell, Ville Simell, Heikki Hyöty, Riitta Veijola, Jorma Ilonen, Marko Sysi-Aho, Mikael Knip, Tuulia Hyötyläinen, Olli Simell

    Research output: Contribution to journalArticleScientificpeer-review

    73 Citations (Scopus)


    Previous studies show that children who later progress to type 1 diabetes (T1D) have decreased preautoimmune concentrations of multiple phospholipids as compared with nonprogressors. It is still unclear whether these changes associate with development of β-cell autoimmunity or specifically with clinical T1D. Here, we studied umbilical cord serum lipidome in infants who later developed T1D (N = 33); infants who developed three or four (N = 31) islet autoantibodies, two (N = 31) islet autoantibodies, or one (N = 48) islet autoantibody during the follow-up; and controls (N = 143) matched for sex, HLA-DQB1 genotype, city of birth, and period of birth. The analyses of serum molecular lipids were performed using the established lipidomics platform based on ultraperformance liquid chromatography coupled to mass spectrometry. We found that T1D progressors are characterized by a distinct cord blood lipidomic profile that includes reduced major cholinecontaining phospholipids, including sphingomyelins and phosphatidylcholines. A molecular signature was developed comprising seven lipids that predicted high risk for progression to T1D with an odds ratio of 5.94 (95% CI, 1.0717.50). Reduction in cholinecontaining phospholipids in cord blood therefore is specifically associated with progression to T1D but not with development of β-cell autoimmunity in general.

    Original languageEnglish
    Pages (from-to)3268-3274
    Issue number9
    Publication statusPublished - 1 Sept 2013
    MoE publication typeA1 Journal article-refereed


    Dive into the research topics of 'Cord serum lipidome in prediction of islet autoimmunity and type 1 diabetes'. Together they form a unique fingerprint.

    Cite this