Fat targeted by type 1 diabetes treatment
Yes, you’re reading that headline correctly; researchers have found that targeting fat could target type 1 diabetes.
Type 1 diabetes is certainly not caused by body fat but what the researchers have found is that fat can be triggered to lower blood glucose levels in another way that does not involve the pancreas’ beta cells.
The researchers, from Vanderbilt University and Washington University, involved 27 mice that were injected with a toxin (streptozocin) that closely mimics type 1 diabetes. The researchers then gave them transplants of brown fat cells (brown adipose tissue or BAT).
The mice were then observed and the researchers noted that sugar levels of the diabetic mice returned to normal. The researchers stated that the brown fat transplants appeared to boost levels of insulin-like growth factor-1 which they believe may have stimulated regeneration of white fat and prompted secretion of hypoglycemic adipokines; that is hormones which can lower blood glucose levels.
New routes towards treating type 1 diabetes
Type 1 diabetes has proved a very difficult condition to cure, despite many attempts being made.
The problem in type 1 diabetes is that the immune system gets locked into thinking that the beta cells, the cells of the pancreas that produce insulin, need to be destroyed. This is a problem because if you try to replace the destroyed beta cells with new ones, the body will still attack these. Adding to the problems is that the immune system is currently too complex for researchers to fully understand and reprogram.
The method employed by the researchers is interesting as it aims to treat type 1 diabetes without either insulin or insulin producing cells. Therefore it is a treatment that may turn out to be unaffected by the key problem presented by the immune system.
The researchers note that there are still challenges ahead as success rates by this method have been lower than have previously been reported. It is certainly a research area that has potential however.
The study appears in the American Journal of Physiology and included funding from the Iacocca Family Foundation.
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