Abstract
IntroductionType 1 diabetes (T1D) is caused by the destruction of pancreatic islet beta cells resulting in total loss of insulin production. Recent studies have suggested that the destruction may be interrelated to plasma lipids.ObjectivesSpecific lipids have previously been shown to be decreased in children who develop T1D before four years of age. Disturbances of plasma lipids prior to clinical diagnosis of diabetes, if true, may provide a novel way to improve prediction, and monitor disease progression.MethodsA lipidomic approach was utilized to analyze plasma from 67 healthy adolescent subjects (10–15 years of age) with or without islet autoantibodies but all with increased genetic risk for T1D. The study subjects were enrolled at birth in the Diabetes Prediction in Skåne (DiPiS) study and after 10–15 years of follow-up we performed the present cross-sectional analysis. HLA-DRB345, -DRB1, -DQA1, -DQB1, -DPA1 and -DPB1 genotypes were determined using next generation sequencing. Lipidomic profiles were determined using ultra-high-performance liquid chromatography quadrupole time-of-flight mass spectrometry. Lipidomics data were analyzed according to genotype.ResultsVariation in levels of several specific phospholipid species were related to level of autoimmunity but not development of T1D. Five glycosylated ceramides were increased in insulin autoantibody (IAA) positive adolescent subjects compared to adolescent subjects without this autoantibody. Additionally, HLA genotypes seemed to influence levels of long chain triacylglycerol (TG).ConclusionLipidomic profiling of adolescent subjects in high risk of T1D may improve sub-phenotyping in this high risk population.
Highlights
Type 1 diabetes (T1D) is caused by the destruction of pancreatic islet beta cells resulting in total loss of insulin production
We further investigate if there are any differences in plasma lipidomic composition in relation to number of islet autoantibodies known to be associated with an increased risk for T1D
Blood samples were collected from adolescent subjects (n = 67), aged 10–15 years, at increased risk of T1D enrolled in the Diabetes Prediction in Skåne (DiPiS) study (Larsson et al 2005; Lundgren et al 2014) as previously described (Andersson Svärd et al 2020) (Table 1)
Summary
Type 1 diabetes (T1D) is caused by the destruction of pancreatic islet beta cells resulting in total loss of insulin production. As in the previously described staging of T1D (Insel et al 2015), progression from multiple autoantibodies (Stage 1) to clinical onset T1D (Stage 3) may be affected by genetic, primarily non-HLA genetic factors, in addition to environmental factors (Söderström et al 2012; Stene et al 2010). It is still unknown how islet autoimmunity is triggered and why some children progress to T1D and others do not
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