Damien Denimal1, Jean-Paul Pais de Barros2, Jean-Michel Petit3, Benjamin Bouillet3, Bruno Vergès3, Laurence Duvillard4. 1. National Institut of Health and Medical Research (INSERM) Unit 866-University Bourgogne-Franche Comté, Bâtiment B3, 15 B(d) M(al) de Lattre de Tassigny, 21000 Dijon, France; Department of Biochemistry, University Hospital, 2 rue Angélique Ducoudray, BP 37013, 21070 Dijon, France. 2. Lipidomic Platform, National Institut of Health and Medical Research (INSERM) Unit 866-University Bourgogne-Franche Comté, Bâtiment B(3), 15 B(d) M(al) de Lattre de Tassigny, 21000 Dijon, France. 3. National Institut of Health and Medical Research (INSERM) Unit 866-University Bourgogne-Franche Comté, Bâtiment B3, 15 B(d) M(al) de Lattre de Tassigny, 21000 Dijon, France; Department of Endocrinology and Metabolic Diseases, University Hospital Bocage Central, 14 rue Gaffarel, 21000 Dijon, France. 4. National Institut of Health and Medical Research (INSERM) Unit 866-University Bourgogne-Franche Comté, Bâtiment B3, 15 B(d) M(al) de Lattre de Tassigny, 21000 Dijon, France; Department of Biochemistry, University Hospital, 2 rue Angélique Ducoudray, BP 37013, 21070 Dijon, France. Electronic address: laurence.duvillard@chu-dijon.fr.
Abstract
OBJECTIVE: Phospholipids and sphingolipids are major components of HDL. They play a critical role in HDL functionality and protective effects against atherosclerosis. As HDL are dysfunctional in type 1 diabetic patients, we ascertained whether they presented abnormalities in their phospholipid and sphingolipid profile, despite normal HDL cholesterol concentration. METHODS: Using liquid chromatography-tandem mass spectrometry, we quantified the main species of phosphatidylcholines, sphingomyelins, lysophophatidylcholines, phosphatidylethanolamines, phosphatidylinositols, ceramides, plasmalogens and sphingosines 1-phosphate in the HDL2 and HDL3 from 54 type 1 diabetic patients and 50 controls. RESULTS: Serum HDL cholesterol was similar in the 2 groups of subjects. When data were expressed relative to the total amount of phospholipids and sphingolipids, sphingosines-1-phosphate (S1P) were 11.7% (NS) and 14.4% (p = 0.0062) lower in HDL2 and HDL3, respectively, from type 1 diabetic patients than from controls. Ceramides were 23% (p = 0.005) and 24% (borderline significance) lower in HDL2 and HDL3, respectively. The concentration of apolipoprotein M, the carrier of S1P, was similar in patients and controls. In type 1 diabetic patients compared to controls, the concentration of d18:1-S1P, the main S1P species, was decreased in total plasma (-17.0%, p < 0.0001), HDL fraction (-21.9%, p < 0.0001) and non-HDL fraction (-13.7%, p = 0.012). The concentration of ceramides was decreased in total plasma (-24.4%, p < 0.0001), HDL fraction (-27.9%, p = 0.0006) and non-HDL fraction (-22.0%, p = 0.0087). CONCLUSION: Despite normal HDL cholesterol level, the phospholipid + sphingolipid profile is impaired in HDL from type 1 diabetic patients. These abnormalities, especially the decrease in S1P, could contribute to the impaired HDL functionality observed in these patients.
OBJECTIVE:Phospholipids and sphingolipids are major components of HDL. They play a critical role in HDL functionality and protective effects against atherosclerosis. As HDL are dysfunctional in type 1 diabeticpatients, we ascertained whether they presented abnormalities in their phospholipid and sphingolipid profile, despite normal HDL cholesterol concentration. METHODS: Using liquid chromatography-tandem mass spectrometry, we quantified the main species of phosphatidylcholines, sphingomyelins, lysophophatidylcholines, phosphatidylethanolamines, phosphatidylinositols, ceramides, plasmalogens and sphingosines 1-phosphate in the HDL2 and HDL3 from 54 type 1 diabeticpatients and 50 controls. RESULTS: Serum HDL cholesterol was similar in the 2 groups of subjects. When data were expressed relative to the total amount of phospholipids and sphingolipids, sphingosines-1-phosphate (S1P) were 11.7% (NS) and 14.4% (p = 0.0062) lower in HDL2 and HDL3, respectively, from type 1 diabeticpatients than from controls. Ceramides were 23% (p = 0.005) and 24% (borderline significance) lower in HDL2 and HDL3, respectively. The concentration of apolipoprotein M, the carrier of S1P, was similar in patients and controls. In type 1 diabeticpatients compared to controls, the concentration of d18:1-S1P, the main S1P species, was decreased in total plasma (-17.0%, p < 0.0001), HDL fraction (-21.9%, p < 0.0001) and non-HDL fraction (-13.7%, p = 0.012). The concentration of ceramides was decreased in total plasma (-24.4%, p < 0.0001), HDL fraction (-27.9%, p = 0.0006) and non-HDL fraction (-22.0%, p = 0.0087). CONCLUSION: Despite normal HDL cholesterol level, the phospholipid + sphingolipid profile is impaired in HDL from type 1 diabeticpatients. These abnormalities, especially the decrease in S1P, could contribute to the impaired HDL functionality observed in these patients.
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