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.

A recent study compared the sperm of 27 men with type 1 diabetes to the sperm of 29 men of equal age without diabetes.

The researchers found that the sperm of the men with diabetes were healthy in many respects. The shape and abundance of the sperm from type 1 diabetic males were perfectly normal and apparently they were great swimmers. However, when the DNA was examined, there was more damage to the DNA of the diabetic men. Around 52% of the DNA in their sperm cells was fragmented, compared to only 32% in the men without diabetes. There was also a higher rate of deletions in the DNA inside their mitochondria, separate DNA found within each cell. The results of this study suggest type 1 diabetes may cause diabetic men to be less fertile.

However Diabetes Health recognizes that many type 1 dads have healthy children - so the study need not be a decision maker or breaker to pursue fatherhood. Thanks to Diabetes Health for reporting the ongoing pursuit of diabetes health.

I know you've always wondered what a diabetes drug might do to a nondiabetic. Riddle solved for this drug- nothing. Dia-B Tech Limited, a Melbourne-based biotech, released results from a medical trial for a new treatment for type 2 diabetes that show it is safe for use in humans without diabetes.

The drug makes a patient's own insulin work better. The insulin sensitizing factor known as compound ISF402 attaches itself to insulin and helps break it down to a more useable form This is a great concept - and one that is fashioned fully in a bitter melon. However, let's give the Aussie biotech the spotlight. Bitter melon is not for the faint of heart - it has teeth!

The study included 24 healthy male volunteers given the treatment and it showed no adverse health effects. If it did not have any effect on healthy individuals - why call it a drug? Call it gum or something mundane. They may have to come up with a whole new category of drug that has no influence in healthy individuals. Maybe they should call it a biologically indifferent agent. Sounds like it still qualifies for a copay, right?

The company now plans to check the treatment's safety on 16 volunteers with type 2 diabetes. The company expects the safety trials to be completed mid-year and then plans to begin a larger trial to find out if the treatment works.

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?

In Diabetes Care this month, researchers report that exposure to agricultural pesticides in the first-trimester increases a woman's risk of developing diabetes during pregnancy.

Researchers assessed the risk of developing gestational diabetes following pesticide exposures among over 11,200 wives of farmers enrolled in the Agricultural Health Study. Within 25 years of entering the study, 4.5% of women who became pregnant reported having gestational diabetes. Overall, 57% of women reported having mixed or applied pesticides at some time in their life, and the proportion was similar for those with and without gestational diabetes mellitus. Women who mixed or applied pesticides or repaired pesticide-related equipment during the first trimester of pregnancy had a more than twofold increased risk of developing gestational diabetes. There was no increased gestational diabetes risk among women with residential exposures to pesticides or indirect exposures during the first trimester.

With the rate of diabetes diagnosis rising, whether it is type 1, type 2 or gestational - understanding the potential effects of environmental exposure on glucose levels is critical to comprehensively addressing the core problem. The jury is still out on deciphering what environmental offense should be sentenced for the crime.

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.