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.
Highlights
Type 1 diabetes (T1D) is an autoimmune disease, characterized by destruction of insulin-producing pancreatic islet β-cells that results in lifelong dependency on exogenous insulin [1]
Our findings have provided further evidence that type 1 diabetes (T1D) progressors have a characteristic lipidomic profile already present at birth
Previous studies have suggested that progression to T1D is associated with decreased concentrations of major phospholipids, including SMs and PCs in cord blood [9,10]
Summary
Type 1 diabetes (T1D) is an autoimmune disease, characterized by destruction of insulin-producing pancreatic islet β-cells that results in lifelong dependency on exogenous insulin [1]. Detection of T1D risk has, become an important area of research, which may inform about potential disease prevention strategies. Several lines of evidence suggest that environmental factors, such as viruses, diet, and gut microbes, may be associated with the initiation of islet autoimmunity and T1D progression [4,5]. It is unlikely that a single factor contributes towards autoimmunity initiation and overt disease. The identification of various endogenous and exogenous contributing factors and their interactions is essential for the early prediction and prevention of T1D
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