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Biomolecules. 2019 Jan 21;9(1). pii: E33. doi: 10.3390/biom9010033.

Cord-Blood Lipidome in Progression to Islet Autoimmunity and Type 1 Diabetes.

Author information

1
Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, 20520 Turku, Finland. santosh.lamichhane@utu.fi.
2
Steno Diabetes Center Copenhagen, 2820 Gentofte, Denmark. la@biosyntia.com.
3
Steno Diabetes Center Copenhagen, 2820 Gentofte, Denmark. thomas@dyrlund.dk.
4
Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, 20520 Turku, Finland. alex.dickens@utu.fi.
5
Children's Hospital, University of Helsinki, Helsinki University Hospital and Research Program Unit, Diabetes and Obesity, University of Helsinki, 00290 Helsinki, Finland. heli.siljander@helsinki.fi.
6
Faculty of Medicine and Life Sciences, University of Tampere, Tampere 33014, Finland. heikki.hyoty@uta.fi.
7
Fimlab Laboratories, Pirkanmaa Hospital District, 33014 Tampere, Finland. heikki.hyoty@uta.fi.
8
Immunogenetics Laboratory, Institute of Biomedicine, University of Turku, 20520 Turku, Finland. jsilonen@utu.fi.
9
Clinical Microbiology, Turku University Hospital, 20014 Turku, Finland. jsilonen@utu.fi.
10
Institute of Biomedicine, Centre for Integrative Physiology and Pharmacology, University of Turku, 20014 Turku, Finland. jortop@utu.fi.
11
Department of Pediatrics, Turku University Hospital, 20521 Turku, Finland. jortop@utu.fi.
12
Department of Pediatrics, PEDEGO Research Unit, Medical Research Centre, University of Oulu, 90014 Oulu, Finland. riitta.veijola@oulu.fi.
13
Department of Children and Adolescents, Oulu University Hospital, 90220 Oulu, Finland. riitta.veijola@oulu.fi.
14
Department of Women's and Children's Health, Karolinska Institutet, 17177 Stockholm, Sweden. riitta.veijola@oulu.fi.
15
School of Science and Technology, Örebro University, 70281 Örebro, Sweden. Tuulia.Hyotylainen@oru.se.
16
Children's Hospital, University of Helsinki, Helsinki University Hospital and Research Program Unit, Diabetes and Obesity, University of Helsinki, 00290 Helsinki, Finland. mikael.knip@helsinki.fi.
17
Tampere Center for Child Health Research, Tampere University Hospital, 33520 Tampere, Finland. mikael.knip@helsinki.fi.
18
Folkhälsan Research Center, 00290 Helsinki, Finland. mikael.knip@helsinki.fi.
19
Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, 20520 Turku, Finland. matej.oresic@utu.fi.
20
School of Medical Sciences, Örebro University, 702 81 Örebro, Sweden. matej.oresic@utu.fi.

Abstract

Previous studies suggest that children who progress to type 1 diabetes (T1D) later in life already have an altered serum lipid molecular profile at birth. Here, we compared cord blood lipidome across the three study groups: children who progressed to T1D (PT1D; n = 30), children who developed at least one islet autoantibody but did not progress to T1D during the follow-up (P1Ab; n = 33), and their age-matched controls (CTR; n = 38). We found that phospholipids, specifically sphingomyelins, were lower in T1D progressors when compared to P1Ab and the CTR. Cholesterol esters remained higher in PT1D when compared to other groups. A signature comprising five lipids was predictive of the risk of progression to T1D, with an area under the receiver operating characteristic curve (AUROC) of 0.83. Our findings provide further evidence that the lipidomic profiles of newborn infants who progress to T1D later in life are different from lipidomic profiles in P1Ab and CTR.

KEYWORDS:

autoimmunity; cord blood; lipidomics; metabolomics; type 1 diabetes

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