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      Sue Tsai; Xavier Clemente-Casares; Xavier S. Revelo; Shawn Winer; Daniel A. Winer

      Disclosures

      Diabetes. 2015;64(6):1886-1897. 

      reverses diabetes type 2 kidshealth (👍 mellitus is primarily a problem with) | reverses diabetes type 2 feethow to reverses diabetes type 2 for Abstract and Introduction

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      Obesity and associated insulin resistance predispose individuals to develop chronic metabolic diseases, such as type 2 diabetes and cardiovascular disease. Although these disorders affect a significant proportion of the global population, the underlying mechanisms of disease remain poorly understood. The discovery of elevated tumor necrosis factor-α in adipose tissue as an inducer of obesity-associated insulin resistance the 1 last update 01 Jun 2020 marked a new era of understanding that a subclinical inflammatory process underlies the insulin resistance and metabolic dysfunction that precedes type 2 diabetes. Advances in the field identified components of both the innate and adaptive immune response as key players in regulating such inflammatory processes. As antigen specificity is a hallmark of an adaptive immune response, its role in modulating the chronic inflammation that accompanies obesity and type 2 diabetes begs the question of whether insulin resistance and type 2 diabetes can have autoimmune components. In this Perspective, we summarize current data that pertain to the activation and perpetuation of adaptive immune responses during obesity and discuss key missing links and potential mechanisms for obesity-related insulin resistance and type 2 diabetes to be considered as potential autoimmune diseases.Obesity and associated insulin resistance predispose individuals to develop chronic metabolic diseases, such as type 2 diabetes and cardiovascular disease. Although these disorders affect a significant proportion of the global population, the underlying mechanisms of disease remain poorly understood. The discovery of elevated tumor necrosis factor-α in adipose tissue as an inducer of obesity-associated insulin resistance marked a new era of understanding that a subclinical inflammatory process underlies the insulin resistance and metabolic dysfunction that precedes type 2 diabetes. Advances in the field identified components of both the innate and adaptive immune response as key players in regulating such inflammatory processes. As antigen specificity is a hallmark of an adaptive immune response, its role in modulating the chronic inflammation that accompanies obesity and type 2 diabetes begs the question of whether insulin resistance and type 2 diabetes can have autoimmune components. In this Perspective, we summarize current data that pertain to the activation and perpetuation of adaptive immune responses during obesity and discuss key missing links and potential mechanisms for obesity-related insulin resistance and type 2 diabetes to be considered as potential autoimmune diseases.

      Introduction

      Traditional autoimmune diseases involve a wide spectrum of clinical pathology and include diseases such as systemic lupus erythematosus, multiple sclerosis, Sjögren''s postulates, originally conceived to establish a causative link between microbes and infectious diseases, to define key criteria that would qualify an autoimmune disease:[1,2]

      1. Evidence of disease-specific adaptive immune response in the affected target tissue or organ

      2. 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

      3. Elimination of the autoimmune response dampens disease progression

      reverses diabetes type 2 foods to avoid (🔴 breakfast recipes) | reverses diabetes type 2 nailshow to reverses diabetes type 2 for Based on the above criteria, diseases with relatively well-established pathophysiology, such as type 1 diabetes and multiple sclerosis, are undisputedly classified as autoimmune. Key autoantigens have been identified and autoreactive specificities have been proven pathogenic through approaches such as adoptive transfer, autoantigen immunization, and transgenesis.[3–6] Loss of tolerance toward self is supported by ample evidence pointing toward defective immune regulation, manifested as a result of combined environmental and predisposing genetic factors.[4,7] Furthermore, researchers have devised immunotherapeutic strategies based on these findings, many of which are being tested clinically as potential treatment for these autoimmune diseases.[8]

      For many other chronic inflammatory conditions, however, the involvement of an autoimmune response in disease development or progression is less clear. Type 2 diabetes and obesity-related insulin resistance are examples of such. Previously thought to be an inflammatory disease mediated predominantly by macrophages infiltrating metabolic tissues, such as the liver and visceral adipose tissue (VAT), obesity-associated adipose inflammation has only recently been tagged as having an adaptive immune component.[9,10] A recent series of studies showed that, similar to macrophages, T and B cells are found to infiltrate the VAT in obese humans and mouse models, with their numbers and inflammatory status closely paralleling the degree of insulin resistance. In addition, alterations in some subclasses of circulating IgGs are also seen during obesity-related insulin resistance.[11] Furthermore, transfer of CD8+ T cells[12,13] or high-fat diet (HFD)-induced IgG antibodies[11] can aggravate insulin resistance without affecting obesity, while T- or B-cell depletion or genetic deficiency improves insulin resistance in diet-induced obese (DIO) mice.[11–14] Through these and other observations, a link between adaptive immunity and obesity-associated inflammation and insulin resistance has been established, and it is now well accepted that adipose tissue inflammation in obesity results from an integrated dialogue between multiple cell types, encompassing metabolic cells as well as both innate and adaptive immune cells. These findings have raised the possibility that obesity-related insulin resistance has a defined autoimmune component to it. Nonetheless, little is known pertaining to the exact nature of the adaptive response mobilized during obesity, such as whether it actively targets self-antigens or foreign antigens, whether it is primarily a bystander, or whether antigen-specific responses are required for β-cell failure in type 2 diabetes. Here, we discuss the potential of obesity-associated inflammation and type 2 diabetes as autoimmune diseases, following the above-mentioned criteria for autoimmunity, and highlight recent clues that will help resolve this intriguing issue.

      Diabetes. 2015;64(6):1886-1897. © 2015  American Diabetes for 1 last update 01 Jun 2020 Association, Inc.
      Diabetes. 2015;64(6):1886-1897. © 2015  American Diabetes Association, Inc.

      References
      Authors and Disclosures

      Authors and Disclosures

      Sue Tsai1, Xavier Clemente-Casares1, Xavier S. Revelo1, Shawn Winer1 and Daniel A. Winer1,2,3,4,5

      reverses diabetes type 2 vs 1 (👍 warning signs) | reverses diabetes type 2 dinner menuhow to reverses diabetes type 2 for 1Division of Cellular and Molecular Biology, Diabetes Research Group, Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
      2Department of Pathology, University Health Network, Toronto, Ontario, Canada
      3Division of Endocrinology and Metabolism, Department of Medicine, University Health Network, Toronto, Ontario, Canada
      4Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
      5Department of Immunology, University of Toronto, Toronto, Ontario, Canada

      Corresponding authors
      Shawn Winer, [email protected], or Daniel A. Winer, [email protected].

      Funding
      Studies of obesity-associated adaptive immune responses in the laboratory of the authors were supported in part by Canadian Institutes of Health Research grant 119414 (D.A.W.), Canadian Diabetes Association grants OG-3-12-3844 and CS-5-12-3886 (D.A.W.), and the University of Toronto Banting & Best Diabetes Centre Sun Life New Investigator Award (D.A.W.). S.T. is a recipient of a Canadian Institutes of Health Research Banting Postdoctoral Fellowship. X.S.R. is the recipient of a Banting & Best Diabetes Centre Fellowship in Diabetes Care (funded by Eli Lilly Canada).

      Duality of Interest
      No potential conflicts of interest relevant to this article were reported.

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