Profile of cardiac lipid metabolism in STZ-induced diabetic mice

Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Li, Wenjie [verfasserIn] Yao, Min Wang, Ruonan Shi, Yun Hou, Lianguo Hou, Ziyuan Lian, Kaoqi Zhang, Nan Wang, Yaqi Li, Weiwei Wang, Wei Jiang, Lingling

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Diabetic myocardial disease Lipotoxicity Non-targeted metabolomics Lipid metabolomics

Anmerkung:	© The Author(s). 2018

Übergeordnetes Werk:	Enthalten in: Lipids in health and disease - London : Biomed Central, 2002, 17(2018), 1 vom: 09. Okt.
Übergeordnetes Werk:	volume:17 ; year:2018 ; number:1 ; day:09 ; month:10

Links:	Volltext

DOI / URN:	10.1186/s12944-018-0872-8

Katalog-ID:	SPR029349230

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520			\|a Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction.
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allfields	10.1186/s12944-018-0872-8 doi (DE-627)SPR029349230 (SPR)s12944-018-0872-8-e DE-627 ger DE-627 rakwb eng Li, Wenjie verfasserin aut Profile of cardiac lipid metabolism in STZ-induced diabetic mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. Diabetic myocardial disease (dpeaa)DE-He213 Lipotoxicity (dpeaa)DE-He213 Non-targeted metabolomics (dpeaa)DE-He213 Lipid metabolomics (dpeaa)DE-He213 Yao, Min aut Wang, Ruonan aut Shi, Yun aut Hou, Lianguo aut Hou, Ziyuan aut Lian, Kaoqi aut Zhang, Nan aut Wang, Yaqi aut Li, Weiwei aut Wang, Wei aut Jiang, Lingling (orcid)0000-0002-2713-7037 aut Enthalten in Lipids in health and disease London : Biomed Central, 2002 17(2018), 1 vom: 09. Okt. (DE-627)355987694 (DE-600)2091381-3 1476-511X nnns volume:17 year:2018 number:1 day:09 month:10 https://dx.doi.org/10.1186/s12944-018-0872-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2018 1 09 10
spelling	10.1186/s12944-018-0872-8 doi (DE-627)SPR029349230 (SPR)s12944-018-0872-8-e DE-627 ger DE-627 rakwb eng Li, Wenjie verfasserin aut Profile of cardiac lipid metabolism in STZ-induced diabetic mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. Diabetic myocardial disease (dpeaa)DE-He213 Lipotoxicity (dpeaa)DE-He213 Non-targeted metabolomics (dpeaa)DE-He213 Lipid metabolomics (dpeaa)DE-He213 Yao, Min aut Wang, Ruonan aut Shi, Yun aut Hou, Lianguo aut Hou, Ziyuan aut Lian, Kaoqi aut Zhang, Nan aut Wang, Yaqi aut Li, Weiwei aut Wang, Wei aut Jiang, Lingling (orcid)0000-0002-2713-7037 aut Enthalten in Lipids in health and disease London : Biomed Central, 2002 17(2018), 1 vom: 09. Okt. (DE-627)355987694 (DE-600)2091381-3 1476-511X nnns volume:17 year:2018 number:1 day:09 month:10 https://dx.doi.org/10.1186/s12944-018-0872-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2018 1 09 10
allfields_unstemmed	10.1186/s12944-018-0872-8 doi (DE-627)SPR029349230 (SPR)s12944-018-0872-8-e DE-627 ger DE-627 rakwb eng Li, Wenjie verfasserin aut Profile of cardiac lipid metabolism in STZ-induced diabetic mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. Diabetic myocardial disease (dpeaa)DE-He213 Lipotoxicity (dpeaa)DE-He213 Non-targeted metabolomics (dpeaa)DE-He213 Lipid metabolomics (dpeaa)DE-He213 Yao, Min aut Wang, Ruonan aut Shi, Yun aut Hou, Lianguo aut Hou, Ziyuan aut Lian, Kaoqi aut Zhang, Nan aut Wang, Yaqi aut Li, Weiwei aut Wang, Wei aut Jiang, Lingling (orcid)0000-0002-2713-7037 aut Enthalten in Lipids in health and disease London : Biomed Central, 2002 17(2018), 1 vom: 09. Okt. (DE-627)355987694 (DE-600)2091381-3 1476-511X nnns volume:17 year:2018 number:1 day:09 month:10 https://dx.doi.org/10.1186/s12944-018-0872-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2018 1 09 10
allfieldsGer	10.1186/s12944-018-0872-8 doi (DE-627)SPR029349230 (SPR)s12944-018-0872-8-e DE-627 ger DE-627 rakwb eng Li, Wenjie verfasserin aut Profile of cardiac lipid metabolism in STZ-induced diabetic mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. Diabetic myocardial disease (dpeaa)DE-He213 Lipotoxicity (dpeaa)DE-He213 Non-targeted metabolomics (dpeaa)DE-He213 Lipid metabolomics (dpeaa)DE-He213 Yao, Min aut Wang, Ruonan aut Shi, Yun aut Hou, Lianguo aut Hou, Ziyuan aut Lian, Kaoqi aut Zhang, Nan aut Wang, Yaqi aut Li, Weiwei aut Wang, Wei aut Jiang, Lingling (orcid)0000-0002-2713-7037 aut Enthalten in Lipids in health and disease London : Biomed Central, 2002 17(2018), 1 vom: 09. Okt. (DE-627)355987694 (DE-600)2091381-3 1476-511X nnns volume:17 year:2018 number:1 day:09 month:10 https://dx.doi.org/10.1186/s12944-018-0872-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2018 1 09 10
allfieldsSound	10.1186/s12944-018-0872-8 doi (DE-627)SPR029349230 (SPR)s12944-018-0872-8-e DE-627 ger DE-627 rakwb eng Li, Wenjie verfasserin aut Profile of cardiac lipid metabolism in STZ-induced diabetic mice 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. Diabetic myocardial disease (dpeaa)DE-He213 Lipotoxicity (dpeaa)DE-He213 Non-targeted metabolomics (dpeaa)DE-He213 Lipid metabolomics (dpeaa)DE-He213 Yao, Min aut Wang, Ruonan aut Shi, Yun aut Hou, Lianguo aut Hou, Ziyuan aut Lian, Kaoqi aut Zhang, Nan aut Wang, Yaqi aut Li, Weiwei aut Wang, Wei aut Jiang, Lingling (orcid)0000-0002-2713-7037 aut Enthalten in Lipids in health and disease London : Biomed Central, 2002 17(2018), 1 vom: 09. Okt. (DE-627)355987694 (DE-600)2091381-3 1476-511X nnns volume:17 year:2018 number:1 day:09 month:10 https://dx.doi.org/10.1186/s12944-018-0872-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 17 2018 1 09 10
language	English
source	Enthalten in Lipids in health and disease 17(2018), 1 vom: 09. Okt. volume:17 year:2018 number:1 day:09 month:10
sourceStr	Enthalten in Lipids in health and disease 17(2018), 1 vom: 09. Okt. volume:17 year:2018 number:1 day:09 month:10
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Diabetic myocardial disease Lipotoxicity Non-targeted metabolomics Lipid metabolomics
isfreeaccess_bool	true
container_title	Lipids in health and disease
authorswithroles_txt_mv	Li, Wenjie @@aut@@ Yao, Min @@aut@@ Wang, Ruonan @@aut@@ Shi, Yun @@aut@@ Hou, Lianguo @@aut@@ Hou, Ziyuan @@aut@@ Lian, Kaoqi @@aut@@ Zhang, Nan @@aut@@ Wang, Yaqi @@aut@@ Li, Weiwei @@aut@@ Wang, Wei @@aut@@ Jiang, Lingling @@aut@@
publishDateDaySort_date	2018-10-09T00:00:00Z
hierarchy_top_id	355987694
id	SPR029349230
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR029349230</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519143921.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2018 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s12944-018-0872-8</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR029349230</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s12944-018-0872-8-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Li, Wenjie</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Profile of cardiac lipid metabolism in STZ-induced diabetic mice</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s). 2018</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Diabetic myocardial disease</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Lipotoxicity</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Non-targeted metabolomics</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Lipid metabolomics</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yao, Min</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Ruonan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shi, Yun</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hou, Lianguo</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hou, Ziyuan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lian, Kaoqi</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Nan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Yaqi</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Weiwei</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Wei</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jiang, Lingling</subfield><subfield code="0">(orcid)0000-0002-2713-7037</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Lipids in health and disease</subfield><subfield code="d">London : Biomed Central, 2002</subfield><subfield code="g">17(2018), 1 vom: 09. 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author	Li, Wenjie
spellingShingle	Li, Wenjie misc Diabetic myocardial disease misc Lipotoxicity misc Non-targeted metabolomics misc Lipid metabolomics Profile of cardiac lipid metabolism in STZ-induced diabetic mice
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topic_title	Profile of cardiac lipid metabolism in STZ-induced diabetic mice Diabetic myocardial disease (dpeaa)DE-He213 Lipotoxicity (dpeaa)DE-He213 Non-targeted metabolomics (dpeaa)DE-He213 Lipid metabolomics (dpeaa)DE-He213
topic	misc Diabetic myocardial disease misc Lipotoxicity misc Non-targeted metabolomics misc Lipid metabolomics
topic_unstemmed	misc Diabetic myocardial disease misc Lipotoxicity misc Non-targeted metabolomics misc Lipid metabolomics
topic_browse	misc Diabetic myocardial disease misc Lipotoxicity misc Non-targeted metabolomics misc Lipid metabolomics
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title	Profile of cardiac lipid metabolism in STZ-induced diabetic mice
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title_full	Profile of cardiac lipid metabolism in STZ-induced diabetic mice
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author_browse	Li, Wenjie Yao, Min Wang, Ruonan Shi, Yun Hou, Lianguo Hou, Ziyuan Lian, Kaoqi Zhang, Nan Wang, Yaqi Li, Weiwei Wang, Wei Jiang, Lingling
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title_sort	profile of cardiac lipid metabolism in stz-induced diabetic mice
title_auth	Profile of cardiac lipid metabolism in STZ-induced diabetic mice
abstract	Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. © The Author(s). 2018
abstractGer	Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. © The Author(s). 2018
abstract_unstemmed	Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction. © The Author(s). 2018
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title_short	Profile of cardiac lipid metabolism in STZ-induced diabetic mice
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up_date	2024-07-04T00:35:50.775Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR029349230</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519143921.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2018 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s12944-018-0872-8</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR029349230</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s12944-018-0872-8-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Li, Wenjie</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Profile of cardiac lipid metabolism in STZ-induced diabetic mice</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s). 2018</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Lipotoxicity contributes to diabetic myocardial disease. In this study, we investigated the lipid species contributing to lipotoxicity and the relationship with peroxisomal β-oxidation in the heart of diabetic mice. Methods Male C57BL/6 mice were randomly divided into a Diabetic group (intraperitoneal injection of STZ) and a Control group (saline). Cardiac function indexes [ejection fraction (EF%) and fractional shortening (FS%)] were evaluated by echocardiography. Morphological changes in the myocardial tissues and mitochondria were assessed by electron microscopy following hematoxylin and eosin staining. Blood myocardial injury indexes and lipids were measured using an automatic biochemical analyzer. Cardiac ATP levels were analyzed using a commercially available kit. mRNA levels of glucose transporter 4 (GLUT4), fatty acid binding protein 3 (FABP3), palmitoyl transferase 1α (CPT-1α), acyl-CoA oxidase 1 (AOX1), D-bifunctional protein (DBP), 3-ketoacyl-CoA thiolase A (THLA), uncoupling protein (UCP) 2 and UCP3 were investigated by quantitative reverse-transcription polymerase chain reaction. FABP3 protein expression was analyzed by Western blotting. Non-targeted metabolomics by LC-MS/MS was applied to evaluate profile of lipid metabolism in heart. Results Compared with controls, EF% and FS% were significantly reduced in diabetic mice. Furthermore, blood myocardial injury indexes and lipids, as well as myocardial mitochondrial cristae fusion were significantly increased. In the diabetic heart, GLUT4 expression was decreased, while expression of FABP3, CPT-1α, AOX1, DBP, THLA, UCP2 and UCP3 was increased, and ATP levels were reduced. In total, 113 lipids exhibited significant differential expression (FC > 2, P < 0.05) between the two groups, with sphingolipid metabolism identified as the top-ranking affected canonical pathway. In the diabetic heart, long-chain hydroxyl-acylcarnitines (8/8) and acylcarnitines (6/11), triglycerides (2/5), and diacyglycerol (3/7) were upregulated, while very long-chain polyunsaturated fatty acids (PUFAs) (5/6) including eicosapentaenoate, docosahexaenoate, phosphocholine (11/19), lysophosphocholine (5/9), phosphoethanolamine (7/11), lysophosphoethanolamine (7/10), phosphatidylglycerol (6/8), phosphoserine (6/8), phosphatidylinositol (2/2), phosphatidic acid (1/1), lysophosphatidic acid (1/1) and sphingomyelin (6/6) were downregulated. Conclusions Our data suggest that the increase in toxic lipid species and decreased in PUFAs undergoing peroxisomal β-oxidation, combined with the reduction in phospholipids cause mitochondrial injury and subsequent uncoupling of phosphorylation and ATP deficiency; thereby leading to diabetic heart dysfunction.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Diabetic myocardial disease</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Lipotoxicity</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Non-targeted metabolomics</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Lipid metabolomics</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yao, Min</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Ruonan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Shi, Yun</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hou, Lianguo</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hou, Ziyuan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lian, Kaoqi</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Nan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Yaqi</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Weiwei</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Wei</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Jiang, Lingling</subfield><subfield code="0">(orcid)0000-0002-2713-7037</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Lipids in health and disease</subfield><subfield code="d">London : Biomed Central, 2002</subfield><subfield code="g">17(2018), 1 vom: 09. 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Profile of cardiac lipid metabolism in STZ-induced diabetic mice

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