Treatment with insulin revolutionized the life of individuals with diabetes. However, because insulin acts to lower blood glucose levels, it can cause hypoglycemia (low levels of glucose in the blood), which, if prolonged, can lead to brain injury and coma.

Extremely prolonged hypoglycemia can cause the death of neurons and irreversible brain damage. In a study appearing in the April issue of the Journal of Clinical Investigation, researchers from the University of California at San Francisco found that in mice, hypoglycemic neuronal death is triggered when the mice are treated with a large amount of glucose and not by the hypoglycemia itself.

Researchers showed that although hypoglycemia induced some neuronal death, the rapid infusion of glucose into hypoglycemic mice triggered more extensive neuronal death. The extent of neuronal death correlated with the production of superoxide by a molecule known as NADPH oxidase. As the amount of glucose infused to treat hypoglycemia increased -- the amount of superoxide produced and the extent of neuronal death was increased. This suggests that it might be best to treat individuals in hypoglycemic coma by gradually increasing their blood glucose levels rather than by restoring glucose levels rapidly. When it comes to recuperating from low sugars -- slow and steady, right Mr. Turtle?

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.