The problem is to find the antigen that drives inflammation. In my view the the higher lipolytic environment during obesity in which the requirement for lipid buffering is elevated, make the macrophage not capable in metabolize all the lipid that is released by over-engorded adipocytes. These will lead to recruitment of more macrophages and release of cytokines, independent of an specific antigen.
The problem is to find the antigen that drives inflammation. In my view the the higher lipolytic environment during obesity in which the requirement for lipid buffering is elevated, make the macrophage not capable in metabolize all the lipid that is released by over-engorded adipocytes. These will lead to recruitment of more macrophages and release of cytokines, independent of an specific antigen.
Obesity arises as a consequence of an interplay between genes, human behaviour and environment. While obesity is on the rise in almost all countries, there are a multitude of factors which might explain this. Obesity is reversible, people change eating and exercise behaviours and convert their BMI to a healthier number. Genetic influences confer increased risk of obesity, not an absolute destiny. Environments have changed dramatically, lifestyles have become more sedentary and stress perhaps more common. Advertising at Christmas would convince you that you should be eating from the top of the food pyramid more. It becomes clear that obesity is a large story. There is much more to it that labelling it an autoimmune disease; which I would not agree with. Perhaps a facet but not the explanation.
There is no scientific data to support that claim. But obesity is considered to be a state of chronic inflammation..and admittedly there is a genetic predisposition issue in addition to environmental factors..
@Salih Sanlioglu I wouldn't say that there is no data to support this notion.
Make sure to read this paper:
Nat Med. 2011 May;17(5):610-7. doi: 10.1038/nm.2353. Epub 2011 Apr 17.
B cells promote insulin resistance through modulation of T cells and production of pathogenic IgG antibodies.
Winer DA, Winer S, Shen L, Wadia PP, Yantha J, Paltser G, Tsui H, Wu P, Davidson MG, Alonso MN, Leong HX, Glassford A, Caimol M, Kenkel JA, Tedder TF, McLaughlin T, Miklos DB, Dosch HM, Engleman EG.
They found that insulin resistance in obese humans is associated with a unique profile of IgG autoantibodies.Most were targeted towards intracellular components that would be released during cell death.
what we have to consider is also the temporality of the immune response. in the later stages, that is true that macrophages tend to become alternatively activated in order to cope with the tissue remodelling. in the early steps of the obesity development, however, I think the literature is sufficiently big to assume the enflamed adipose tissue is a major source of Th1 cytokines...
As mentionned by Philip, emerging data question a role of autoimmunity (see also Cell Metabolism 17, 411–422, March 5, 2013; and Immunity. 2012 Sep 21;37(3):574-87)
Obesity results in Low grade chronic inflammation and thus could be consider as an autoimmune disease.
Additionally, there is some evidence that those afflicted with autoimmune diseases are more prone to weight gain
Dear Michael
Obesity is often associated with cardiovascular disease and diabetes .
Less known is the connection between excess weight and autoimmune diseases , where the immune system starts to attack the body itself. This knowledge is now expanding with the discovery of how this autoimmune response occurs - how to stop it .
The key may be in an element known as AMI ( inhibitor of apoptosis in macrophages ) - Apoptosis is programmed cell death, and macrophages are cells of the immune system .
Toru Miyazaki and his colleagues at Tokyo University have identified AMI ( inhibitor of apoptosis in macrophages ) in the bloodstream , associating it with the inflammation that occurs in tissues generated by obesity .
In obesity , the MI - IgM complex , which activates autoimmunity is retained in the blood, rather than being excreted in the urine.
They found that the suppression of AMI - can allow cells to be able to reschedule his death normally - can also prevent autoimmune diseases .
"Our study explained , for the first time as obesity causes an initial autoimmune response, including the production of antibodies against various self antigens, and also defines a key molecule in this autoimmune process , " Miyazaki said .
The researchers found that a natural immunoglobulin IgM call increases in blood fed a high-fat diet mice. The increase in IgM result of stimuli that induce fatty acids on immune cells . Furthermore, the IgM binds to AMI, and this complex is retained in the blood, rather than being excreted in the urine.
They concluded that prolonged IgM AMI blood contributes to the production of autoantibodies .
" Thus, inhibition of AMI can be used as a therapy to prevent not only insulin resistance and metabolic disorders, autoimmunity but also in conditions of obesity, " Miyazaki
Below some articles may be helpful for you:
1) Metabolic syndrome: variations on the theme of inflammation.
Miyazaki T.
Semin Immunopathol. 2014 Jan;36(1):
2) Impacts of the apoptosis inhibitor of macrophage (AIM) on obesity-associated inflammatory diseases.
Arai S, Miyazaki T.
Semin Immunopathol. 2014 Jan;36(1):.
3) Latest topics on macrophage-derived AIM -multiple AIM roles in obesity-associated diseases].
Arai S, Miyazaki T.
Nihon Rinsho. 2013 Sep;71(9):1681-9.
4) Obesity-associated autoantibody production requires AIM to retain the immunoglobulin M immune complex on follicular dendritic cells.
Arai S, Maehara N, Iwamura Y, Honda S, Nakashima K, Kai T, Ogishi M, Morita K, Kurokawa J, Mori M, Motoi Y, Miyake K, Matsuhashi N, Yamamura K, Ohara O, Shibuya A, Wakeland EK, Li QZ, Miyazaki T.
Cell Rep. 2013 Apr 25;3(4):1187-98
.
Fei and Zhao in a paper in Nature showed that morbid obesity was the result of a large population of Klebsiella mobilis (only they used the old name which I can't remember) in the gut. They cured the problem by giving a diet of whole grain and Chinese medicinal vegetables which reduced the K mobilis population to normal levels. Some obesity is clearly an actual disease.
Obesity has been associated with decreased Treg and
B-regulatory subsets, expansion of Th17 cells, and promotion of autoantibodies.
Altogether, these mechanisms may lead to a breakdown of
self-tolerance, promoting the development of autoimmunity and
subsequent autoimmune disease.
Let's suppose that obesity is an autoimmune disease, can we treat or stop it by the conventional regimes of autoimmune disease treatment. If the answer is yes, the answer of your question will be yes.
Hello,
Obesity is not an autoimmune disease. Actually genetic and environmental factors with bad nutritional habits and sedentary life leading to obesity and its related complications.
مة. Obesity may be a genetic disease and therefore difficult to control and the factors causing it, and may lead to heart disease, atherosclerosis and hypertension. Obesity may be due to unhealthy eating habits, including high intake of fatty foods, sweets and high calorie foods, Food value
Obesity is not a autoimmune disease, but it plays major role in triggering autoimmune diseases. Please take a look at the following references.
Article Obesity as a Risk and Severity Factor in Rheumatic Diseases ...
Article Body mass index and risk of autoimmune diseases: A study wit...
Article Overweight, obesity and the risk of LADA: results from a Swe...
Autoimmune diseases like Crohn's Disease and multiple sclerosis, in which the immune system attacks its own body rather than predatory invaders, affect 5-20% of the global community. A study published recently in Autoimmunity Reviews by Prof. Yehuda Shoenfeld, the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases at Tel Aviv University's Sackler Faculty of Medicine and Head of Zabludowicz Center for Autoimmune Diseases at Chaim Sheba Medical Center, Tel Hashomer, points to the major role obesity plays in triggering and prolonging these autoimmune diseases.
Please follow this useful link:
https://www.sciencedaily.com/releases/2014/11/141110110722.htm
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