Specific Hepatic Sphingolipids Relate to Insulin Resistance, Oxidative Stress, and Inflammation in Nonalcoholic Steatohepatitis

Insulin resistance and nonalcoholic fatty liver disease have been linked to several lipid metabolites in animals, but their role in humans remains unclear. This study examined the relationship of sphingolipids with hepatic and peripheral metabolism in 21 insulin-resistant obese patients without (NAF...

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Vydané v:Diabetes care Ročník 41; číslo 6; s. 1235
Hlavní autori: Apostolopoulou, Maria, Gordillo, Ruth, Koliaki, Chrysi, Gancheva, Sofia, Jelenik, Tomas, De Filippo, Elisabetta, Herder, Christian, Markgraf, Daniel, Jankowiak, Frank, Esposito, Irene, Schlensak, Matthias, Scherer, Philipp E, Roden, Michael
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 01.06.2018
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ISSN:1935-5548, 1935-5548
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Abstract Insulin resistance and nonalcoholic fatty liver disease have been linked to several lipid metabolites in animals, but their role in humans remains unclear. This study examined the relationship of sphingolipids with hepatic and peripheral metabolism in 21 insulin-resistant obese patients without (NAFL-) or with (NAFL+) nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH) and 7 healthy lean individuals undergoing tissue biopsies during bariatric or elective abdominal surgery. Hyperinsulinemic-euglycemic clamps with d-[6,6- H ]glucose were performed to quantify tissue-specific insulin sensitivity. Hepatic oxidative capacity, lipid peroxidation, and the phosphorylated-to-total c-Jun N-terminal kinase (pJNK-to-tJNK) ratio were measured to assess mitochondrial function, oxidative stress, and inflammatory activity. Hepatic total ceramides were higher by 50% and 33% in NASH compared with NAFL+ and NAFL-, respectively. Only in NASH were hepatic dihydroceramides (16:0, 22:0, and 24:1) and lactosylceramides increased. Serum total ceramides and dihydroceramides (hepatic dihydroceramides 22:0 and 24:1) correlated negatively with whole-body but not with hepatic insulin sensitivity. Hepatic maximal respiration related positively to serum lactosylceramide subspecies, hepatic sphinganine, and lactosylceramide 14:0. Liver lipid peroxides (total ceramides, sphingomyelin 22:0) and the pJNK-to-tJNK ratio (ceramide 24:0; hexosylceramides 22:0, 24:0, and 24:1) all positively correlated with the respective hepatic sphingolipids. Sphingolipid species are not only increased in insulin-resistant humans with NASH but also correlate with hepatic oxidative stress and inflammation, suggesting that these lipids may play a role during progression of simple steatosis to NASH in humans.
AbstractList Insulin resistance and nonalcoholic fatty liver disease have been linked to several lipid metabolites in animals, but their role in humans remains unclear. This study examined the relationship of sphingolipids with hepatic and peripheral metabolism in 21 insulin-resistant obese patients without (NAFL-) or with (NAFL+) nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH) and 7 healthy lean individuals undergoing tissue biopsies during bariatric or elective abdominal surgery.OBJECTIVEInsulin resistance and nonalcoholic fatty liver disease have been linked to several lipid metabolites in animals, but their role in humans remains unclear. This study examined the relationship of sphingolipids with hepatic and peripheral metabolism in 21 insulin-resistant obese patients without (NAFL-) or with (NAFL+) nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH) and 7 healthy lean individuals undergoing tissue biopsies during bariatric or elective abdominal surgery.Hyperinsulinemic-euglycemic clamps with d-[6,6-2H2]glucose were performed to quantify tissue-specific insulin sensitivity. Hepatic oxidative capacity, lipid peroxidation, and the phosphorylated-to-total c-Jun N-terminal kinase (pJNK-to-tJNK) ratio were measured to assess mitochondrial function, oxidative stress, and inflammatory activity.RESEARCH DESIGN AND METHODSHyperinsulinemic-euglycemic clamps with d-[6,6-2H2]glucose were performed to quantify tissue-specific insulin sensitivity. Hepatic oxidative capacity, lipid peroxidation, and the phosphorylated-to-total c-Jun N-terminal kinase (pJNK-to-tJNK) ratio were measured to assess mitochondrial function, oxidative stress, and inflammatory activity.Hepatic total ceramides were higher by 50% and 33% in NASH compared with NAFL+ and NAFL-, respectively. Only in NASH were hepatic dihydroceramides (16:0, 22:0, and 24:1) and lactosylceramides increased. Serum total ceramides and dihydroceramides (hepatic dihydroceramides 22:0 and 24:1) correlated negatively with whole-body but not with hepatic insulin sensitivity. Hepatic maximal respiration related positively to serum lactosylceramide subspecies, hepatic sphinganine, and lactosylceramide 14:0. Liver lipid peroxides (total ceramides, sphingomyelin 22:0) and the pJNK-to-tJNK ratio (ceramide 24:0; hexosylceramides 22:0, 24:0, and 24:1) all positively correlated with the respective hepatic sphingolipids.RESULTSHepatic total ceramides were higher by 50% and 33% in NASH compared with NAFL+ and NAFL-, respectively. Only in NASH were hepatic dihydroceramides (16:0, 22:0, and 24:1) and lactosylceramides increased. Serum total ceramides and dihydroceramides (hepatic dihydroceramides 22:0 and 24:1) correlated negatively with whole-body but not with hepatic insulin sensitivity. Hepatic maximal respiration related positively to serum lactosylceramide subspecies, hepatic sphinganine, and lactosylceramide 14:0. Liver lipid peroxides (total ceramides, sphingomyelin 22:0) and the pJNK-to-tJNK ratio (ceramide 24:0; hexosylceramides 22:0, 24:0, and 24:1) all positively correlated with the respective hepatic sphingolipids.Sphingolipid species are not only increased in insulin-resistant humans with NASH but also correlate with hepatic oxidative stress and inflammation, suggesting that these lipids may play a role during progression of simple steatosis to NASH in humans.CONCLUSIONSSphingolipid species are not only increased in insulin-resistant humans with NASH but also correlate with hepatic oxidative stress and inflammation, suggesting that these lipids may play a role during progression of simple steatosis to NASH in humans.
Insulin resistance and nonalcoholic fatty liver disease have been linked to several lipid metabolites in animals, but their role in humans remains unclear. This study examined the relationship of sphingolipids with hepatic and peripheral metabolism in 21 insulin-resistant obese patients without (NAFL-) or with (NAFL+) nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH) and 7 healthy lean individuals undergoing tissue biopsies during bariatric or elective abdominal surgery. Hyperinsulinemic-euglycemic clamps with d-[6,6- H ]glucose were performed to quantify tissue-specific insulin sensitivity. Hepatic oxidative capacity, lipid peroxidation, and the phosphorylated-to-total c-Jun N-terminal kinase (pJNK-to-tJNK) ratio were measured to assess mitochondrial function, oxidative stress, and inflammatory activity. Hepatic total ceramides were higher by 50% and 33% in NASH compared with NAFL+ and NAFL-, respectively. Only in NASH were hepatic dihydroceramides (16:0, 22:0, and 24:1) and lactosylceramides increased. Serum total ceramides and dihydroceramides (hepatic dihydroceramides 22:0 and 24:1) correlated negatively with whole-body but not with hepatic insulin sensitivity. Hepatic maximal respiration related positively to serum lactosylceramide subspecies, hepatic sphinganine, and lactosylceramide 14:0. Liver lipid peroxides (total ceramides, sphingomyelin 22:0) and the pJNK-to-tJNK ratio (ceramide 24:0; hexosylceramides 22:0, 24:0, and 24:1) all positively correlated with the respective hepatic sphingolipids. Sphingolipid species are not only increased in insulin-resistant humans with NASH but also correlate with hepatic oxidative stress and inflammation, suggesting that these lipids may play a role during progression of simple steatosis to NASH in humans.
Author Gancheva, Sofia
Roden, Michael
Schlensak, Matthias
Esposito, Irene
Jelenik, Tomas
Markgraf, Daniel
Koliaki, Chrysi
De Filippo, Elisabetta
Jankowiak, Frank
Apostolopoulou, Maria
Scherer, Philipp E
Gordillo, Ruth
Herder, Christian
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  organization: German Center for Diabetes Research, München-Neuherberg, Germany
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  fullname: Gordillo, Ruth
  organization: Touchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX
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  surname: Koliaki
  fullname: Koliaki, Chrysi
  organization: German Center for Diabetes Research, München-Neuherberg, Germany
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  fullname: Gancheva, Sofia
  organization: German Center for Diabetes Research, München-Neuherberg, Germany
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  orcidid: 0000-0002-2061-1162
  surname: Jelenik
  fullname: Jelenik, Tomas
  organization: German Center for Diabetes Research, München-Neuherberg, Germany
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  organization: German Center for Diabetes Research, München-Neuherberg, Germany
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  givenname: Christian
  orcidid: 0000-0002-2050-093X
  surname: Herder
  fullname: Herder, Christian
  organization: German Center for Diabetes Research, München-Neuherberg, Germany
– sequence: 8
  givenname: Daniel
  surname: Markgraf
  fullname: Markgraf, Daniel
  organization: German Center for Diabetes Research, München-Neuherberg, Germany
– sequence: 9
  givenname: Frank
  surname: Jankowiak
  fullname: Jankowiak, Frank
  organization: Institute of Pathology, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany
– sequence: 10
  givenname: Irene
  surname: Esposito
  fullname: Esposito, Irene
  organization: Institute of Pathology, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany
– sequence: 11
  givenname: Matthias
  surname: Schlensak
  fullname: Schlensak, Matthias
  organization: General Surgery Department, Schön Clinic, Düsseldorf, Germany
– sequence: 12
  givenname: Philipp E
  orcidid: 0000-0002-5336-1358
  surname: Scherer
  fullname: Scherer, Philipp E
  organization: Touchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX
– sequence: 13
  givenname: Michael
  orcidid: 0000-0001-8200-6382
  surname: Roden
  fullname: Roden, Michael
  email: michael.roden@ddz.uni-duesseldorf.de
  organization: German Center for Diabetes Research, München-Neuherberg, Germany
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29602794$$D View this record in MEDLINE/PubMed
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Copyright 2018 by the American Diabetes Association.
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PublicationTitle Diabetes care
PublicationTitleAlternate Diabetes Care
PublicationYear 2018
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Snippet Insulin resistance and nonalcoholic fatty liver disease have been linked to several lipid metabolites in animals, but their role in humans remains unclear....
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SubjectTerms Adult
Animals
Disease Progression
Female
Glucose Clamp Technique
Humans
Inflammation - blood
Inflammation - metabolism
Inflammation - physiopathology
Insulin Resistance - physiology
Lipid Peroxidation - physiology
Liver - chemistry
Liver - metabolism
Liver - pathology
Male
Middle Aged
Non-alcoholic Fatty Liver Disease - blood
Non-alcoholic Fatty Liver Disease - metabolism
Non-alcoholic Fatty Liver Disease - physiopathology
Obesity - blood
Obesity - metabolism
Obesity - physiopathology
Obesity - surgery
Oxidation-Reduction
Oxidative Stress - physiology
Prospective Studies
Sphingolipids - analysis
Sphingolipids - blood
Sphingolipids - metabolism
Title Specific Hepatic Sphingolipids Relate to Insulin Resistance, Oxidative Stress, and Inflammation in Nonalcoholic Steatohepatitis
URI https://www.ncbi.nlm.nih.gov/pubmed/29602794
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