Skip to main content
  • American Heart Association
  • Science Volunteer
  • Warning Signs
  • Advanced Search
  • Donate

  • Home
  • About this Journal
    • Editorial Board
    • Meet the Editors
    • ATVB Journal History
    • General Statistics
  • All Issues
  • Subjects
    • All Subjects
    • Arrhythmia and Electrophysiology
    • Basic, Translational, and Clinical Research
    • Critical Care and Resuscitation
    • Epidemiology, Lifestyle, and Prevention
    • Genetics
    • Heart Failure and Cardiac Disease
    • Hypertension
    • Imaging and Diagnostic Testing
    • Intervention, Surgery, Transplantation
    • Quality and Outcomes
    • Stroke
    • Vascular Disease
  • Browse Features
    • Cover Art Award
    • ATVB Early Career Award
    • ATVB in Focus
    • Recent Brief Reviews of ATVB
    • Lecture Series
    • Collections
    • Recent Highlights of ATVB
    • Commentaries
    • Browse Abstracts
    • Insight into ATVB Authors
  • Resources
    • Instructions for Authors
    • Online Submission/Peer Review Site
    • Council on ATVB
    • Permissions and Rights Q&A
    • AHA Guidelines and Statements
    • Customer Service and Ordering Information
    • Author Reprints
    • International Users
    • AHA Newsroom
  • AHA Journals
    • AHA Journals Home
    • Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)
    • Circulation
    • → Circ: Arrhythmia and Electrophysiology
    • → Circ: Genomic and Precision Medicine
    • → Circ: Cardiovascular Imaging
    • → Circ: Cardiovascular Interventions
    • → Circ: Cardiovascular Quality & Outcomes
    • → Circ: Heart Failure
    • Circulation Research
    • Hypertension
    • Stroke
    • Journal of the American Heart Association
  • Facebook
  • LinkedIn
  • Twitter

  • My alerts
  • Sign In
  • Join

  • Advanced search

Header Publisher Menu

  • American Heart Association
  • Science Volunteer
  • Warning Signs
  • Advanced Search
  • Donate

Arteriosclerosis, Thrombosis, and Vascular Biology

  • My alerts
  • Sign In
  • Join

  • Facebook
  • LinkedIn
  • Twitter
  • Home
  • About this Journal
    • Editorial Board
    • Meet the Editors
    • ATVB Journal History
    • General Statistics
  • All Issues
  • Subjects
    • All Subjects
    • Arrhythmia and Electrophysiology
    • Basic, Translational, and Clinical Research
    • Critical Care and Resuscitation
    • Epidemiology, Lifestyle, and Prevention
    • Genetics
    • Heart Failure and Cardiac Disease
    • Hypertension
    • Imaging and Diagnostic Testing
    • Intervention, Surgery, Transplantation
    • Quality and Outcomes
    • Stroke
    • Vascular Disease
  • Browse Features
    • Cover Art Award
    • ATVB Early Career Award
    • ATVB in Focus
    • Recent Brief Reviews of ATVB
    • Lecture Series
    • Collections
    • Recent Highlights of ATVB
    • Commentaries
    • Browse Abstracts
    • Insight into ATVB Authors
  • Resources
    • Instructions for Authors
    • Online Submission/Peer Review Site
    • Council on ATVB
    • Permissions and Rights Q&A
    • AHA Guidelines and Statements
    • Customer Service and Ordering Information
    • Author Reprints
    • International Users
    • AHA Newsroom
  • AHA Journals
    • AHA Journals Home
    • Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)
    • Circulation
    • → Circ: Arrhythmia and Electrophysiology
    • → Circ: Genomic and Precision Medicine
    • → Circ: Cardiovascular Imaging
    • → Circ: Cardiovascular Interventions
    • → Circ: Cardiovascular Quality & Outcomes
    • → Circ: Heart Failure
    • Circulation Research
    • Hypertension
    • Stroke
    • Journal of the American Heart Association
Atherosclerosis/Lipoproteins

Lack of Invariant Natural Killer T Cells Affects Lipid Metabolism in Adipose Tissue of Diet-Induced Obese Mice

Daniela Strodthoff, Anna M. Lundberg, Hanna E. Agardh, Daniel F.J. Ketelhuth, Gabrielle Paulsson-Berne, Peter Arner, Göran K. Hansson, Norbert Gerdes
Download PDF
https://doi.org/10.1161/ATVBAHA.112.301105
Arteriosclerosis, Thrombosis, and Vascular Biology. 2013;ATVBAHA.112.301105
Originally published March 21, 2013
Daniela Strodthoff
From the Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden (D.S., A.M.L., H.E.A., D.F.J.K., G.P.-B., G.K.H., N.G.); Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden (P.A.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.); and Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands (N.G.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Anna M. Lundberg
From the Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden (D.S., A.M.L., H.E.A., D.F.J.K., G.P.-B., G.K.H., N.G.); Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden (P.A.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.); and Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands (N.G.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Hanna E. Agardh
From the Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden (D.S., A.M.L., H.E.A., D.F.J.K., G.P.-B., G.K.H., N.G.); Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden (P.A.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.); and Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands (N.G.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Daniel F.J. Ketelhuth
From the Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden (D.S., A.M.L., H.E.A., D.F.J.K., G.P.-B., G.K.H., N.G.); Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden (P.A.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.); and Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands (N.G.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Gabrielle Paulsson-Berne
From the Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden (D.S., A.M.L., H.E.A., D.F.J.K., G.P.-B., G.K.H., N.G.); Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden (P.A.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.); and Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands (N.G.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Peter Arner
From the Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden (D.S., A.M.L., H.E.A., D.F.J.K., G.P.-B., G.K.H., N.G.); Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden (P.A.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.); and Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands (N.G.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Göran K. Hansson
From the Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden (D.S., A.M.L., H.E.A., D.F.J.K., G.P.-B., G.K.H., N.G.); Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden (P.A.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.); and Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands (N.G.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Norbert Gerdes
From the Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden (D.S., A.M.L., H.E.A., D.F.J.K., G.P.-B., G.K.H., N.G.); Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institute, Stockholm, Sweden (P.A.); Institute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University (LMU), Munich, Germany (N.G.); and Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, The Netherlands (N.G.).
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Supplemental Materials
  • Info & Metrics
  • eLetters

Jump to

  • Article
  • Supplemental Materials
  • Info & Metrics
  • eLetters
Loading

Abstract

Objective—Obesity promotes a chronic inflammatory condition in adipose tissue (AT). Impairment of insulin sensitivity coincides with infiltration of T cells into AT in early stages of obesity, when macrophages are not yet present. Here, we examine the role of invariant natural killer T (iNKT) cells, a subtype of T cells activated by lipid antigens, on glucose and lipid metabolism in obesity.

Approach and Results—Jα18−/− mice, specifically lacking iNKT cells, and wild-type mice consumed a chow or high-fat diet for 10 weeks. One third of all T lymphocytes in the liver of wild-type mice were iNKT cells, whereas few were detected in AT. Diet-induced obesity increased blood glucose in both genotypes of mice, whereas glucose tolerance test revealed similar kinetics of glucose clearance in Jα18−/− and wild-type mice. Under obese conditions, expression of inflammatory cytokines in AT did not differ between the groups, although the number of T cells and macrophages was lower in Jα18−/− mice. Nonetheless, AT homeostasis in Jα18−/− mice was altered evidenced by lower AT weight, smaller adipocytes, accelerated lipogenesis, increased expression of hormone-sensitive lipase, and accelerated basal lipolysis.

Conclusions—iNKT cells do not affect glucose clearance but rather modulate lipid metabolism in both liver and AT. Only few iNKT cells are found in AT under lean and obese conditions, suggesting that their effects on lipid metabolism are mainly mediated in the liver, their primary host organ.

  • immune system
  • leukocytes
  • lipases
  • NKT cells
  • obesity
  • Received December 30, 2012.
  • Accepted February 26, 2013.
  • © 2013 American Heart Association, Inc.
Back to top
Next Article

Current Issue

Arteriosclerosis, Thrombosis, and Vascular Biology
April 2018, Volume 38, Issue 4
  • Table of Contents
Next Article

Jump to

  • Article
  • Supplemental Materials
  • Info & Metrics
  • eLetters

Article Tools

  • Print
  • Citation Tools
    Lack of Invariant Natural Killer T Cells Affects Lipid Metabolism in Adipose Tissue of Diet-Induced Obese Mice
    Daniela Strodthoff, Anna M. Lundberg, Hanna E. Agardh, Daniel F.J. Ketelhuth, Gabrielle Paulsson-Berne, Peter Arner, Göran K. Hansson and Norbert Gerdes
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2013;ATVBAHA.112.301105, originally published March 21, 2013
    https://doi.org/10.1161/ATVBAHA.112.301105

    Citation Manager Formats

    • BibTeX
    • Bookends
    • EasyBib
    • EndNote (tagged)
    • EndNote 8 (xml)
    • Medlars
    • Mendeley
    • Papers
    • RefWorks Tagged
    • Ref Manager
    • RIS
    • Zotero
  • Article Alerts
    Log in to Email Alerts with your email address.
  • Save to my folders

Share this Article

  • Email

    Thank you for your interest in spreading the word on Arteriosclerosis, Thrombosis, and Vascular Biology.

    NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

    Enter multiple addresses on separate lines or separate them with commas.
    Lack of Invariant Natural Killer T Cells Affects Lipid Metabolism in Adipose Tissue of Diet-Induced Obese Mice
    (Your Name) has sent you a message from Arteriosclerosis, Thrombosis, and Vascular Biology
    (Your Name) thought you would like to see the Arteriosclerosis, Thrombosis, and Vascular Biology web site.
  • Share on Social Media
    Lack of Invariant Natural Killer T Cells Affects Lipid Metabolism in Adipose Tissue of Diet-Induced Obese Mice
    Daniela Strodthoff, Anna M. Lundberg, Hanna E. Agardh, Daniel F.J. Ketelhuth, Gabrielle Paulsson-Berne, Peter Arner, Göran K. Hansson and Norbert Gerdes
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2013;ATVBAHA.112.301105, originally published March 21, 2013
    https://doi.org/10.1161/ATVBAHA.112.301105
    del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo

Related Articles

Cited By...

Subjects

  • Epidemiology, Lifestyle, and Prevention
    • Diabetes, Type 2
  • Basic, Translational, and Clinical Research
    • Animal Models of Human Disease

Arteriosclerosis, Thrombosis, and Vascular Biology

  • About ATVB
  • AHA CME
  • Meeting Abstracts
  • Permissions
  • Email Alerts
  • Open Access Information
  • AHA Journals RSS
  • AHA Newsroom

Contact the Editorial Office:
email: atvb@atvb.org

Information for:
  • Advertisers
  • Subscribers
  • Subscriber Help
  • Institutions / Librarians
  • Institutional Subscriptions FAQ
  • International Users
American Heart Association Learn and Live
National Center
7272 Greenville Ave.
Dallas, TX 75231

Customer Service

  • 1-800-AHA-USA-1
  • 1-800-242-8721
  • Local Info
  • Contact Us

About Us

Our mission is to build healthier lives, free of cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question. Find Out More about the American Heart Association

  • Careers
  • SHOP
  • Latest Heart and Stroke News
  • AHA/ASA Media Newsroom

Our Sites

  • American Heart Association
  • American Stroke Association
  • For Professionals
  • More Sites

Take Action

  • Advocate
  • Donate
  • Planned Giving
  • Volunteer

Online Communities

  • AFib Support
  • Garden Community
  • Patient Support Network
  • Professional Online Network

Follow Us:

  • Follow Circulation on Twitter
  • Visit Circulation on Facebook
  • Follow Circulation on Google Plus
  • Follow Circulation on Instagram
  • Follow Circulation on Pinterest
  • Follow Circulation on YouTube
  • Rss Feeds
  • Privacy Policy
  • Copyright
  • Ethics Policy
  • Conflict of Interest Policy
  • Linking Policy
  • Diversity
  • Careers

©2018 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. The American Heart Association is a qualified 501(c)(3) tax-exempt organization.
*Red Dress™ DHHS, Go Red™ AHA; National Wear Red Day ® is a registered trademark.

  • PUTTING PATIENTS FIRST National Health Council Standards of Excellence Certification Program
  • BBB Accredited Charity
  • Comodo Secured