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Perspectives in Diabetes

Are Obesity-Related Insulin Resistance and Type 2 Diabetes Autoimmune Diseases?

  1. Sue Tsai1,
  2. Xavier Clemente-Casares1,
  3. Xavier S. Revelo1,
  4. Shawn Winer1⇑ and
  5. Daniel A. Winer1,2,3,4,5⇑
  1. 1Division of Cellular and Molecular Biology, Diabetes Research Group, Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
  2. 2Department of Pathology, University Health Network, Toronto, Ontario, Canada
  3. 3Division of Endocrinology and Metabolism, Department of Medicine, University Health Network, Toronto, Ontario, Canada
  4. 4Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
  5. 5Department of Immunology, University of Toronto, Toronto, Ontario, Canada
  1. Corresponding authors: Shawn Winer, shawn.winer{at}utoronto.ca, or Daniel A. Winer, dan.winer{at}uhn.ca
Diabetes 2015 Jun; 64(6): 1886-1897. https://doi.org/10.2337/db14-1488
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    Figure 1

    Evidence of autoreactivity in T1D and T2D according to modified postulates. Due to the extensive literature describing type 1 diabetes pathogenesis, we reference a number of review articles that can point readers to primary literatures on the different aspects. IR, insulin resistance.

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    Figure 2

    Proposed pathways, centered in the VAT, to autoimmune responses during obesity. Intrinsic inflammatory changes cooperate with obesity-associated dysbiosis in the gut to initiate self- or microbe-specific adaptive immune responses in the VAT, generating a feed-forward inflammatory loop that worsens insulin signaling. Long-term caloric excess causes hypertrophy and ER stress in white adipocytes, leading to the release of adipokines and chemoattractants that help activate and/or recruit innate cells, such as macrophages, and adaptive immune cells, such as B and T cells, to the VAT. Obesity-associated dysbiosis contributes to increased gut permeability, facilitating leakage of microbial products and oral antigens across the gut epithelium. Together with lipid excess and dying adipocytes, these serve as potential sources of antigens and costimulatory signals for the activation of VAT B and T cells, a process that can potentially take place in the draining lymph nodes or locally in the VAT. Activated B and T cells, in turn, contribute to VAT inflammation through the secretion of inflammatory cytokines and antibodies or through cross talk with other immune cells. DAMPs, danger-associated molecular patterns. PAMPs, pathogen-associated molecular patterns.

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June 2015, 64(6)
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Are Obesity-Related Insulin Resistance and Type 2 Diabetes Autoimmune Diseases?
Sue Tsai, Xavier Clemente-Casares, Xavier S. Revelo, Shawn Winer, Daniel A. Winer
Diabetes Jun 2015, 64 (6) 1886-1897; DOI: 10.2337/db14-1488

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Are Obesity-Related Insulin Resistance and Type 2 Diabetes Autoimmune Diseases?
Sue Tsai, Xavier Clemente-Casares, Xavier S. Revelo, Shawn Winer, Daniel A. Winer
Diabetes Jun 2015, 64 (6) 1886-1897; DOI: 10.2337/db14-1488
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    • Introduction
    • Evidence of Disease-Specific Adaptive Immune Response in the Affected Target Tissue or Organ
    • Demonstration of the Ability of Autoreactive T and B Cells and/or Autoantibodies to Transfer Disease to Healthy Individuals or Animals Through Adoptive Transfer or Autoantigen Immunization
    • Elimination of the Autoimmune Response Dampens Disease Progression
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    • Are Obesity-Related Insulin Resistance and Type 2 Diabetes Autoimmune Diseases?
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