Up-Regulation of Specific Bioactive Lipids in Celiac Disease
Celiac disease (CD) is an autoimmune enteropathy linked to alterations of metabolism. Currently, limited untargeted metabolomic studies evaluating differences in the plasma metabolome of CD subjects have been documented. We engage in a metabolomic study that analyzes plasma metabolome in 17 children...
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Published in | Nutrients Vol. 13; no. 7; p. 2271 |
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Main Authors | , , , , , , , |
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Abstract | Celiac disease (CD) is an autoimmune enteropathy linked to alterations of metabolism. Currently, limited untargeted metabolomic studies evaluating differences in the plasma metabolome of CD subjects have been documented. We engage in a metabolomic study that analyzes plasma metabolome in 17 children with CD treated with a gluten-free diet and 17 healthy control siblings in order to recognize potential changes in metabolic networks. Our data demonstrates the persistence of metabolic defects in CD subjects in spite of the dietary treatment, affecting a minor but significant fraction (around 4%, 209 out of 4893 molecular features) of the analyzed plasma metabolome. The affected molecular species are mainly, but not exclusively, lipid species with a particular affectation of steroids and derivatives (indicating an adrenal gland affectation), glycerophospholipids (to highlight phosphatidic acid), glycerolipids (with a special affectation of diacylglycerols), and fatty acyls (eicosanoids). Our findings are suggestive of an activation of the diacylglycerol-phosphatidic acid signaling pathway in CD that may potentially have detrimental effects via activation of several targets including protein kinases such as mTOR, which could be the basis of the morbidity and mortality connected with untreated CD. However, more studies are necessary to validate this idea regarding CD. |
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AbstractList | Celiac disease (CD) is an autoimmune enteropathy linked to alterations of metabolism. Currently, limited untargeted metabolomic studies evaluating differences in the plasma metabolome of CD subjects have been documented. We engage in a metabolomic study that analyzes plasma metabolome in 17 children with CD treated with a gluten-free diet and 17 healthy control siblings in order to recognize potential changes in metabolic networks. Our data demonstrates the persistence of metabolic defects in CD subjects in spite of the dietary treatment, affecting a minor but significant fraction (around 4%, 209 out of 4893 molecular features) of the analyzed plasma metabolome. The affected molecular species are mainly, but not exclusively, lipid species with a particular affectation of steroids and derivatives (indicating an adrenal gland affectation), glycerophospholipids (to highlight phosphatidic acid), glycerolipids (with a special affectation of diacylglycerols), and fatty acyls (eicosanoids). Our findings are suggestive of an activation of the diacylglycerol-phosphatidic acid signaling pathway in CD that may potentially have detrimental effects via activation of several targets including protein kinases such as mTOR, which could be the basis of the morbidity and mortality connected with untreated CD. However, more studies are necessary to validate this idea regarding CD. Celiac disease (CD) is an autoimmune enteropathy linked to alterations of metabolism. Currently, limited untargeted metabolomic studies evaluating differences in the plasma metabolome of CD subjects have been documented. We engage in a metabolomic study that analyzes plasma metabolome in 17 children with CD treated with a gluten-free diet and 17 healthy control siblings in order to recognize potential changes in metabolic networks. Our data demonstrates the persistence of metabolic defects in CD subjects in spite of the dietary treatment, affecting a minor but significant fraction (around 4%, 209 out of 4893 molecular features) of the analyzed plasma metabolome. The affected molecular species are mainly, but not exclusively, lipid species with a particular affectation of steroids and derivatives (indicating an adrenal gland affectation), glycerophospholipids (to highlight phosphatidic acid), glycerolipids (with a special affectation of diacylglycerols), and fatty acyls (eicosanoids). Our findings are suggestive of an activation of the diacylglycerol-phosphatidic acid signaling pathway in CD that may potentially have detrimental effects via activation of several targets including protein kinases such as mTOR, which could be the basis of the morbidity and mortality connected with untreated CD. However, more studies are necessary to validate this idea regarding CD.Celiac disease (CD) is an autoimmune enteropathy linked to alterations of metabolism. Currently, limited untargeted metabolomic studies evaluating differences in the plasma metabolome of CD subjects have been documented. We engage in a metabolomic study that analyzes plasma metabolome in 17 children with CD treated with a gluten-free diet and 17 healthy control siblings in order to recognize potential changes in metabolic networks. Our data demonstrates the persistence of metabolic defects in CD subjects in spite of the dietary treatment, affecting a minor but significant fraction (around 4%, 209 out of 4893 molecular features) of the analyzed plasma metabolome. The affected molecular species are mainly, but not exclusively, lipid species with a particular affectation of steroids and derivatives (indicating an adrenal gland affectation), glycerophospholipids (to highlight phosphatidic acid), glycerolipids (with a special affectation of diacylglycerols), and fatty acyls (eicosanoids). Our findings are suggestive of an activation of the diacylglycerol-phosphatidic acid signaling pathway in CD that may potentially have detrimental effects via activation of several targets including protein kinases such as mTOR, which could be the basis of the morbidity and mortality connected with untreated CD. However, more studies are necessary to validate this idea regarding CD. |
Audience | Academic |
Author | Pamplona, Reinald Jové, Mariona Nestares, Teresa Mota-Martorell, Natàlia Sol, Joaquim Martín-Masot, Rafael Galo-Licona, Jose Maldonado, José |
AuthorAffiliation | 2 Department of Experimental Medicine, Lleida Biomedical Research Institute (IRBLleida), University of Lleida (UdL), 25198 Lleida, Spain; jgalolic25@gmail.com (J.D.G.-L.); nataliamotamartorell@gmail.com (N.M.-M.); jsol.lleida.ics@gencat.cat (J.S.); mariona.jove@udl.cat (M.J.); reinald.pamplona@udl.cat (R.P.) 1 Pediatric Gastroenterology and Nutrition Unit, Hospital Regional Universitario de Malaga, 29011 Málaga, Spain 7 Maternal and Child Health Network, Carlos III Health Institute, 28029 Madrid, Spain 8 Biomedical Research Centre (CIBM), Department of Physiology and “José MataixVerdú”, Institute of Nutrition and Food Technology (INYTA), University of Granada, 18071 Granada, Spain; nestares@ugr.es 3 Institut Català de la Salut, Atenció Primària, 25198 Lleida, Spain 5 Department of Pediatrics, University of Granada, 18071 Granada, Spain; jmaldon@ugr.es 4 Research Support Unit Lleida, Fundació Institut Universitari per a la Recerca a l’Atenció Primària de Salut Jordi Gol i Gurina (IDIAPJGol), |
AuthorAffiliation_xml | – name: 1 Pediatric Gastroenterology and Nutrition Unit, Hospital Regional Universitario de Malaga, 29011 Málaga, Spain – name: 3 Institut Català de la Salut, Atenció Primària, 25198 Lleida, Spain – name: 8 Biomedical Research Centre (CIBM), Department of Physiology and “José MataixVerdú”, Institute of Nutrition and Food Technology (INYTA), University of Granada, 18071 Granada, Spain; nestares@ugr.es – name: 6 Pediatric Gastroenterology and Nutrition Unit, Hospital Universitario Virgen de las Nieves, 18071 Granada, Spain – name: 5 Department of Pediatrics, University of Granada, 18071 Granada, Spain; jmaldon@ugr.es – name: 7 Maternal and Child Health Network, Carlos III Health Institute, 28029 Madrid, Spain – name: 2 Department of Experimental Medicine, Lleida Biomedical Research Institute (IRBLleida), University of Lleida (UdL), 25198 Lleida, Spain; jgalolic25@gmail.com (J.D.G.-L.); nataliamotamartorell@gmail.com (N.M.-M.); jsol.lleida.ics@gencat.cat (J.S.); mariona.jove@udl.cat (M.J.); reinald.pamplona@udl.cat (R.P.) – name: 4 Research Support Unit Lleida, Fundació Institut Universitari per a la Recerca a l’Atenció Primària de Salut Jordi Gol i Gurina (IDIAPJGol), 25198 Lleida, Spain |
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SubjectTerms | adrenal glands Celiac disease Chromatography Diabetes diacylglycerols Discriminant analysis Disease eicosanoids Gastroenterology gluten-free diet glycerophospholipids Hepatology Instrument industry Lipids Metabolism Metabolites metabolome metabolomics morbidity mortality NMR Nuclear magnetic resonance Nutrition nutritional intervention Particle size Plasma Principal components analysis protein kinases Quality control Retention Siblings Software |
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Title | Up-Regulation of Specific Bioactive Lipids in Celiac Disease |
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