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Salk Institute calls for type 4 diabetes classification following insulin resistance findings

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New research finds diabetes or insulin resistance in older mice has a different cellular cause than diabetes caused by obesity. The findings, published in the journal Nature, call for a new kind of diabetes classification: type 4 diabetes. The study was conducted by co-leading scientists Ronald Evans and Ye Zheng, both of the Salk Institute, United States. Evans is director of Salk Institute's Gene Expression Laboratory, while Zheng is an associate professor at Salk's Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis. Evans wanted to investigate why thin, older people can develop type 2 diabetes without weight gain. The research team compared the immune systems of healthy mice, those with obesity-related insulin resistance and those with age-related insulin resistance. They found that levels of regulatory T cells inside fat tissue (Tregs) were abnormally higher in mice with age-related diabetes. Conversely, mice with obesity-related diabetes had normal levels of Tregs, despite having more fat tissue. The researchers explained that while Tregs can help calm inflammation, they gradually accumulate within fat as someone ages. If the cells completely block inflammation in fat tissue, this causes fat deposits building around and inside body parts such as the liver, which can lead to insulin resistance. When the researchers blocked Treg cells in the mice, they no longer developed age-associated insulin resistance (type 4 diabetes) in old age. Blocking Treg cells in obese mice did not prevent obesity-related insulin resistance. Evans said: "A lot of diabetes in the elderly goes undiagnosed because they don't have the classical risk factors for type 2 diabetes, such as obesity. It turns out that for this type of diabetes, the treatment is not losing weight. The treatment is actually losing these cells, and we show that it's possible to do that. "We hope our discovery not only leads to therapeutics, but to an increased recognition of type 4 diabetes as a distinct disease." Evans and Zheng's team now plan to work out how Tregs interact with fat tissue and if immune cells accelerate in other organs during normal aging. They also want to conduct these studies in humans to see if the results are similar.

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Bingo. A glimmer of understanding of my condition and why it seems to be different from so many other people's on here. I've always felt, without any evidence, that impacted internal fat was at least part cause of my T2 and that my aim should be to disperse it. I regarded myself as a toffee (TOFI - thin outside, fat inside). I have wondered for some time if high intensity interval training
http://www.diabetes.co.uk/high-intensity-interval-training.html could aid dispersal of internal fat. Dr Mike Mosley suggested as such in one of his tv programmes a while back.
I'll be following the Salk programme.
 
Yes, I shall be following the Salk Institute, as this is the category I think I fit the best. My consultant agreed in 2010 that there was a possibility of LADA but the GAD test was negative. My GP's computer system could classify me only as a type 2, despite there being no classical markers such as overweight/obesity, hypertension and hypercholesterolaemia.
I did read an interesting Lancet paper from Dec 2013 "The many faces of diabetes: a disease with increasing heterogenicity". However, the Evans and Zheng work does throw a lot of light on what could well be an under-recognised disease and gives hope that curative immunotherapy could become available.
 
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This fits the diabetes that has hit 3 generations of my family, on my father's side. All slim. All fit. All active. All developed 'T2' in their 60s-70s.

There are other factors at work with me but I kind of suspect that my sister and I have this too. Will be very curious to follow this research in the future.
 
Doesn't tell you how to block Tregs, though.
There was also an article this year saying that obesity reduced the number of Tregs and too few Tregs led to inflammation and T2.
So too many or too few are bad.
Edit: so should skinny T2s (T4s?) eat more to create new fat which doesn't have a high concentration of Treg?
 
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