Conventional wisdom holds that Type 1 diabetes is an autoimmune condition — caused by a misguided attack by the immune system on the beta cells of the pancreas — while Type 2 diabetes is not, caused instead by a combination of genes and lifestyle. Experts have debated the relative importance of genes, lifestyle, and environmental factors in the development of Type 2 diabetes — and at times, studies linking Type 2 diabetes to pollution and toxins have fueled speculation that autoimmunity plays a role in its development. But until this month, there was little conclusive evidence of an autoimmune role in Type 2 diabetes.
That changed last week, with the release of a study that addressed the potential connection between autoimmunity and Type 2 diabetes head-on. Published on the Web site of the journal Nature Medicine, the study had two components: one in humans, and one in mice. As described in a HealthDay article, for the mouse experiment, researchers fed mice a high-fat diet that would be expected to induce insulin resistance, a hallmark of Type 2 diabetes in humans. After five weeks, they gave some of the mice a drug, known as anti-CD20, that suppresses the immune system by depleting a type of immune system cell known as B cells. In mice given the drug, there was no sign of insulin resistance, and blood glucose levels were normal. All of the other mice developed insulin resistance. This result suggests that in overweight mice — and, most likely, humans — an immune system attack on fat cells, instigated by B cells, leads to insulin resistance.
Conducting a similar experiment in humans would be much more complicated, both pragmatically and ethically, since the drug anti-CD20 (known as rituximab when intended for humans) broadly suppresses the immune system, not just autoimmune attacks on fat cells. So to test whether the mice findings might also apply to humans, the researchers took blood samples from 32 obese people, half of whom had insulin resistance. The blood samples were screened for antibodies — proteins created by the immune system to attack specific substances — and the researchers found that distinctly different sets of antibodies were present in participants with and without insulin resistance. While this result does not have the same scientific weight as an intervention study (in which participants are randomly assigned to a treatment), it does suggest that autoimmunity plays a role in insulin resistance in humans. Further research could possibly lead to new therapies for Type 2 diabetes that address autoimmunity, or to prevention efforts if environmental triggers of autoimmunity — such as chemicals or pollution — can be linked to diabetes.
What do you think — if you have Type 2 diabetes, are you pleased to see new evidence that you didn’t “bring it on yourself” simply by being overweight or obese? Given that many toxins and chemicals are associated with autoimmunity, do you suspect that any of these might have contributed to your diabetes? Do you think this study will inspire a new sense of solidarity between people with Type 1 and Type 2 diabetes, now that both conditions appear to involve autoimmunity — or will some rancor between the two groups continue? Leave a comment below!
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