We've long known about Type 1 diabetes. Most people know about Type 2 diabetes, too. But would you believe it's possible that a discovery may warrant a Type 3 diabetes? Researchers have discovered that the suppression of insulin signaling in the brain raises the possibility of a Type 3 diabetes.

Researchers have known for some time that insulin is not just produced in the pancreas, but also in the thymus. It is also known that insulin resistance, a characteristic of Type 2 diabetes, is tied to neurodegeneration. While scientists have suspected a link between diabetes and Alzheimer's disease, this is the first study to provide evidence of that connection. The study identified a gene abnormality that blocks insulin signaling in the brain. A drop in insulin production in the thymus contributes to the degeneration of specific regions of the brain. These abnormalities do not correspond to Type 1 or Type 2 diabetes, but reflect a different and more complex disease process that originates in the CNS (central nervous system). This raises the possibility of a Type 3 diabetes.

Those who suffered from Alzheimer's disease had a deficiency of growth factor in the hippocampus. The hippocampus is the part of the brain responsible for memory. The absence of these growth factors causes cells in other parts of the brain to die. Reserachers found that insulin was significantly reduced in the areas of the brain responsible for reasoning, planning, speech, movement, emotions, and problem solving. Researchers conclude that there is a genuine need for comprehensive study of the neuropathological changes associated with diabetes treatment and the affects of specific medications on insulin signaling. I agree with the researchers!

Scientists have found that mice lacking a protein known as SH2B1 throughout their body are obese and ultimately develop diabetes. Researchers replaced SH2B1 in the brain of obese mice and it seemed to deter the onset of obesity. The study reveals that targeting SH2B1 in the brain might be a new avenue of treatments for obesity and type 2 diabetes.

SH2B1 is expressed in tissues related to obesity, including the brain, liver, pancreas, and fat tissue. Replacing SH2B1 in the brain of mice lacking SH2B1 prevented the mice from becoming obese. It also prevented the mice from developing obesity after being fed a high-fat diet, indicating that SH2B1 in the brain is required to regulate body weight and fat content.

This study implies that SH2B1 in the brain is a practical target for the development of new drugs to treat obesity and type 2 diabetes.

Richard Kahn, Chief Scientific & Medical Officer for the American Diabetes Association, is blogging the American Diabetes Association's 66th Annual Scientific Sessions. From June 9 - 13, the annual convention brings together leading scientists and health professionals to present the latest study findings and to discuss the current and future progress in the field of diabetes prevention and care.

So far, some of Kahn's posts have covered such topics as: insulin and longevity; endocannabinoids, oral insulin, the new A1C test, who is responsible for optimal diabetes care; the worm study; and you are what your mother ate during her pregnancy. The posting is written in a light and easy manner, not requiring the average person to being a textbook of medical definitions to make sense out of what is being said. I assume Kahn will continue blogging through June 13. You can read Richard's D.C. Diary here.