A type 1 diabetic mystery is why do some Type 1s get complications and others seem to never get them? A massive Japanese study of Type 1 diabetics found that those with fulminant diabetes developed complications much faster and more severely than those with non-fulminant diabetes.

The difference between fulminant and non-fulminant is the speed and intensity at which the disease develops. Fulminant Type 1 diabetes typically develops suddenly with near total loss of beta cell function. This type of diabetes is confirmed with testing c-peptide levels. Non-fulminant type 1 diabetes has residual c-peptide levels that eventually taper to undetectable. Sometimes this is seen through many years of the Honeymoon Period.

This study may be the antithesis of conventional wisdom for preventing complications. Staking all hopes on blood sugar control is heavily optimistic. Yes controlling blood sugar does lessen the workload for existing beta cells, and thus extends the lifespan of each beta cell. Research suggests that c-peptide offers protection to beta cells, both from apoptosis (cell death) and encourages new cell growth. This new cell growth applies to beta cells and other cells of the body that endure long-term Type 1 diabetes complications.

Diabetics are instructed that maintaining normal blood sugars is the Holy Grail of preventing long-term complications. Yes and no. The truth is controlling your blood sugar will not allow complications of Type 1 diabetes to develop as quickly, presuming you still had some level of beta cell function upon diagnosis (i.e., c-peptide). That doesn't sound like a reward as much as it does a delayed punishment. I'd like c-peptide with my insulin, please. It's off the à la carte menu? That's fine - serve it up! I want to thank Klausen for bringing this study to my attention.

Japanese scientists have discovered an imbalance that leads to the development of type 2 diabetes in mice. A gene called GCK is responsible for sensing changes in blood glucose levels. Researchers found a molecule known as insulin receptor substrate 2 (IRS2) was shown to influence the beta cell mass increase after GCK sensed an increased in blood glucose levels.

The Journal of Clinical Investigation focused on mice with little increase in beta cell mass regardless of a rise in GCK. Researchers found, in healthy mice, the insulin receptor substrate 2 (IRS2) was shown to influence the beta cell mass increase after GCK first sensed an increased in blood glucose levels.

Before a person becomes diabetic, his or her body tries to compensate for the increasing resistance to insulin by upping the amount of insulin secreted and the mass of insulin-secreting cells (beta cells) in the pancreas. Researchers will look for new ways of increasing beta cell mass to prevent the onset of type 2 diabetes. Here's where I get a little confused - another study conducted a few years ago found evidence that a sucrose-rich diet (SRD) produces an increase in the pancreatic beta-cell mass in the rat. I'm neither a rat, nor a scientist - but I think a meeting of the minds behind these two discoveries might result in some forward-thinking treatments for type 2 diabetes. What compels the IRS2 to defy the command center of GCK? Perhaps another piece is missing from the balance of this equation.