A longitudinal plasma lipidomics dataset from children who developed islet autoimmunity and type 1 diabetes

Early prediction and prevention of type 1 diabetes (T1D) are currently unmet medical needs. Previous metabolomics studies suggest that children who develop T1D are characterised by a distinct metabolic profile already detectable during infancy, prior to the onset of islet autoimmunity. However, the specificity of persistent metabolic disturbances in relation T1D development has not yet been established. Here, we report a longitudinal plasma lipidomics dataset from (1) 40 children who progressed to T1D during follow-up, (2) 40 children who developed single islet autoantibody but did not develop T1D and (3) 40 matched controls (6 time points: 3, 6, 12, 18, 24 and 36 months of age). This dataset may help other researchers in studying age-dependent progression of islet autoimmunity and T1D as well as of the age-dependence of lipidomic profiles in general. Alternatively, this dataset could more broadly used for the development of methods for the analysis of longitudinal multivariate data.Peer reviewe

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

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

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

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.Peer reviewe

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

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

Dynamics of Plasma Lipidome in Progression to Islet Autoimmunity and Type 1 Diabetes - Type 1 Diabetes Prediction and Prevention Study (DIPP)

Type 1 diabetes (T1D) is one of the most prevalent autoimmune diseases among children in Western countries. Earlier metabolomics studies suggest that T1D is preceded by dysregulation of lipid metabolism. Here we used a lipidomics approach to analyze molecular lipids in a prospective series of 428 plasma samples from 40 children who progressed to T1D (PT1D), 40 children who developed at least a single islet autoantibody but did not progress to T1D during the follow-up (P1Ab) and 40 matched controls (CTR). Sphingomyelins were found to be persistently downregulated in PT1D when compared to the P1Ab and CTR groups. Triacylglycerols and phosphatidylcholines were mainly downregulated in PT1D as compared to P1Ab at the age of 3 months. Our study suggests that distinct lipidomic signatures characterize children who progressed to islet autoimmunity or overt T1D, which may be helpful in the identification of at-risk children before the initiation of autoimmunity

Dynamics of Plasma Lipidome in Progression to Islet Autoimmunity and Type 1 Diabetes - Type 1 Diabetes Prediction and Prevention Study (DIPP)

Type 1 diabetes (T1D) is one of the most prevalent autoimmune diseases among children in Western countries. Earlier metabolomics studies suggest that T1D is preceded by dysregulation of lipid metabolism. Here we used a lipidomics approach to analyze molecular lipids in a prospective series of 428 plasma samples from 40 children who progressed to T1D (PT1D), 40 children who developed at least a single islet autoantibody but did not progress to T1D during the follow-up (P1Ab) and 40 matched controls (CTR). Sphingomyelins were found to be persistently downregulated in PT1D when compared to the P1Ab and CTR groups. Triacylglycerols and phosphatidylcholines were mainly downregulated in PT1D as compared to P1Ab at the age of 3 months. Our study suggests that distinct lipidomic signatures characterize children who progressed to islet autoimmunity or overt T1D, which may be helpful in the identification of at-risk children before the initiation of autoimmunity.Peer reviewe

A longitudinal plasma lipidomics dataset from children who developed islet autoimmunity and type 1 diabetes

Abstract Early prediction and prevention of type 1 diabetes (T1D) are currently unmet medical needs. Previous metabolomics studies suggest that children who develop T1D are characterised by a distinct metabolic profile already detectable during infancy, prior to the onset of islet autoimmunity. However, the specificity of persistent metabolic disturbances in relation T1D development has not yet been established. Here, we report a longitudinal plasma lipidomics dataset from (1) 40 children who progressed to T1D during follow-up, (2) 40 children who developed single islet autoantibody but did not develop T1D and (3) 40 matched controls (6 time points: 3, 6, 12, 18, 24 and 36 months of age). This dataset may help other researchers in studying age-dependent progression of islet autoimmunity and T1D as well as of the age-dependence of lipidomic profiles in general. Alternatively, this dataset could more broadly used for the development of methods for the analysis of longitudinal multivariate data

Cord-blood lipidome in progression to islet autoimmunity and type 1 diabetes

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

mzmine/mzmine3: Latest Development Build

<h2>Commits</h2> <ul> <li>05f944a: Dont allow multivariate curve resolution module on macos (kyrasolaris01) <a href="https://github.com/mzmine/mzmine3/pull/1613">#1613</a></li> <li>9307519: Increment patch version (SteffenHeu)</li> <li>2de4d07: Use SystemUtils for OS detection (kyrasolaris01) <a href="https://github.com/mzmine/mzmine3/pull/1613">#1613</a></li> <li>bbd6b08: Use features not peaks in ADAP decon parameters (kyrasolaris01) <a href="https://github.com/mzmine/mzmine3/pull/1613">#1613</a></li> </ul&gt

mzmine/mzmine3: Latest Development Build

<h2>Commits</h2> <ul> <li>d963958: add iintest ions, fix ion type in csv search (Steffen Heuckeroth) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>b2a64df: fix notation (Steffen Heuckeroth) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>71785a0: fix ion parsing for special cases with electrons (robinschmid) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>0c433cb: Merge remote-tracking branch 'SteffenHeu/add-more-ions-to-iintest' into fork/add-more-ions-to-iintest (robinschmid) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>25c5f53: add special ion case (robinschmid) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>b01e966: Merge remote-tracking branch 'mzmine/master' into add-more-ions-to-iintest (Steffen Heuckeroth) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>0b4a328: Merge remote-tracking branch 'origin/add-more-ions-to-iintest' into add-more-ions-to-iintest (Steffen Heuckeroth) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>26f90c5: handle null in number parsing (robinschmid) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>96a18f4: Merge remote-tracking branch 'SteffenHeu/add-more-ions-to-iintest' into fork/add-more-ions-to-iintest (robinschmid) <a href="https://github.com/mzmine/mzmine3/pull/1610">#1610</a></li> <li>b72438d: Increment patch version (ansgarkorf)</li> </ul&gt