Natural killer T cells in adipose tissue prevent insulin resistance
Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased i...
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| Veröffentlicht in: | The Journal of clinical investigation Jg. 122; H. 9; S. 3343 - 3354 |
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| Hauptverfasser: | , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
United States
American Society for Clinical Investigation
01.09.2012
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| ISSN: | 0021-9738, 1558-8238, 1558-8238 |
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| Abstract | Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance. |
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| AbstractList | Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance.Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance. Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance. Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance. [PUBLICATION ABSTRACT] |
| Audience | Academic |
| Author | Nieuwenhuis, Edward E.S. Venken, Koen Hamers, Nicole Besra, Gurdyal Prakken, Berent Boes, Marianne Prop, Serge van de Graaf, Stan F.J. Koppen, Arjen Boon, Louis Rakhshandehroo, Maryam Meerding, Jenny Stienstra, Rinke Elewaut, Dirk Schipper, Henk S. Kersten, Sander Kalkhoven, Eric |
| AuthorAffiliation | 1 Department of Metabolic Diseases, University Medical Center Utrecht, Utrecht, the Netherlands. 2 Department of Pediatric Immunology and Infectious Diseases, University Medical Center Utrecht and Center for Molecular and Cellular Intervention, University Medical Center Utrecht, Wilhelmina Children’s Hospital, Utrecht, the Netherlands. 3 Netherlands Metabolomics Center, Leiden, the Netherlands. 4 Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University, Ghent, Belgium. 5 Nutrition, Metabolism, and Genomics Group, Division of Human Nutrition, Wageningen University, Wageningen, the Netherlands. 6 Department of Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands. 7 School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom. 8 Bioceros BV, Utrecht, the Netherlands |
| AuthorAffiliation_xml | – name: 1 Department of Metabolic Diseases, University Medical Center Utrecht, Utrecht, the Netherlands. 2 Department of Pediatric Immunology and Infectious Diseases, University Medical Center Utrecht and Center for Molecular and Cellular Intervention, University Medical Center Utrecht, Wilhelmina Children’s Hospital, Utrecht, the Netherlands. 3 Netherlands Metabolomics Center, Leiden, the Netherlands. 4 Department of Rheumatology, Faculty of Medicine and Health Sciences, Laboratory for Molecular Immunology and Inflammation, Ghent University, Ghent, Belgium. 5 Nutrition, Metabolism, and Genomics Group, Division of Human Nutrition, Wageningen University, Wageningen, the Netherlands. 6 Department of Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands. 7 School of Biosciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom. 8 Bioceros BV, Utrecht, the Netherlands |
| Author_xml | – sequence: 1 givenname: Henk S. surname: Schipper fullname: Schipper, Henk S. – sequence: 2 givenname: Maryam surname: Rakhshandehroo fullname: Rakhshandehroo, Maryam – sequence: 3 givenname: Stan F.J. surname: van de Graaf fullname: van de Graaf, Stan F.J. – sequence: 4 givenname: Koen surname: Venken fullname: Venken, Koen – sequence: 5 givenname: Arjen surname: Koppen fullname: Koppen, Arjen – sequence: 6 givenname: Rinke surname: Stienstra fullname: Stienstra, Rinke – sequence: 7 givenname: Serge surname: Prop fullname: Prop, Serge – sequence: 8 givenname: Jenny surname: Meerding fullname: Meerding, Jenny – sequence: 9 givenname: Nicole surname: Hamers fullname: Hamers, Nicole – sequence: 10 givenname: Gurdyal surname: Besra fullname: Besra, Gurdyal – sequence: 11 givenname: Louis surname: Boon fullname: Boon, Louis – sequence: 12 givenname: Edward E.S. surname: Nieuwenhuis fullname: Nieuwenhuis, Edward E.S. – sequence: 13 givenname: Dirk surname: Elewaut fullname: Elewaut, Dirk – sequence: 14 givenname: Berent surname: Prakken fullname: Prakken, Berent – sequence: 15 givenname: Sander surname: Kersten fullname: Kersten, Sander – sequence: 16 givenname: Marianne surname: Boes fullname: Boes, Marianne – sequence: 17 givenname: Eric surname: Kalkhoven fullname: Kalkhoven, Eric |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22863618$$D View this record in MEDLINE/PubMed |
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| Copyright | COPYRIGHT 2012 American Society for Clinical Investigation Copyright American Society for Clinical Investigation Sep 2012 Copyright © 2012, American Society for Clinical Investigation 2012 Wageningen University & Research |
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| Title | Natural killer T cells in adipose tissue prevent insulin resistance |
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