For quite some time, many researchers and lay people alike have subscribed to what is known as the "Thrifty Genotype Theory." Basically, this theory suggests that cycles of feast and famine that occurred early in human history created a gene that assists the body in utilizing scarce nutrients.

Because we as humans no longer operate on a feast or famine eating cycle, however, this gene -- which still remains -- leads to obesity and diabetes. In addition, this theory pointed to certain ethnic groups; Native Americans, Mexican Americans, African Americans, Australian Aborigine and other indigenous groups as being genetically prone to diabetes because of their link to this particular gene.

In efforts to challenge the ethnic presumptions, and erode the "Thrifty Genotype Theory" altogether, a study by U.S. and Australian researchers examines existing genetic studies published across a variety of disciplines. Whereas past studies into the genetic link to diabetes failed to control for outside variables, this new study factors in poverty, housing segregation and poor diet -- and, upon completion of the researchers' analysis, all were found to be stronger indicators of diabetes than genes.

Knocking out the gene for a peptide associated with insulin was shown to protect mice against the harmful effects of a high-fat diet. Urocortin 3 plays a role in the increased production of insulin in response to high caloric intake in animals.

Scientists found that by removing the urocortin 3 gene from mice, they did not develop the age-related insulin resistance and high blood sugar observed in the normal control mice. The metabolisms of normal mice were compared to the metabolisms of those without the urocortin 3 gene. When placed on a high caloric diet for three months, the mice without the urocortin 3 gene packed on the same amount of weight but had lower insulin levels. But these mice also had lower blood sugar, improved glucose tolerance curves and they did not develop the fatty livers the control mice experienced.

Scientists hypothesize that by curtailing the abnormally high insulin levels, they were able to manipulate insulin sensitivity and avoid some of the untoward consequences of the high food intake and weight gain. Like many of us diabetics already know too well - while insulin is effective at lowering blood sugar it also promotes fat storage. This is a natural protective response to prepare for times when food may not be available. When insulin is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organs.

Urocortin 2 and urocortin 3 are part of the system that governs the body's response to insulin. Scientists already know that mice on a high-fat diet do better if either urocortin 2 or urocortin 3 is removed. Now they want to know if the mice will respond even better if both are missing. Such results may instruct us how best to develop therapeutic means to exploit these powerful effects.

Scientists in Germany are reporting development of a urine test that finally can identify athletes who misuse certain kinds of insulin in an illicit attempt to enhance performance.

An article scheduled to appear in an April edition of Analytical Chemistry says it is possible to detect the misuse of insulin in a urine sample. Scientists had not attempted to develop a test in the past because of the presumption that it was impossible to detect misuses of insulin. Because insulin is rationed and used efficiently by the body, a byproduct of insulin would be theoretically undetectable. However, with the advent of the newer long-acting insulin analogues, scientists are now able to identify degradation product in the urine.

The test does not identify residue from the use of two other forms of long-duration insulin. However, the test does identify the misuse of Lantus, manufactured by Sanofi-aventis. Determination of long-acting insulin analogues in urine is especially helpful for doping control purposes. The procedure provides a fast and reliable way to identify the misuse of the long-acting insulin analogue LAN in regular doping control specimens.

According to scientists at Washington University School of Medicine in St. Louis, interrupting nerve signals to the liver can prevent diabetes and hypertension in mice.

Mice were treated to become diabetic with glucocorticoids, a class of steroid hormones characterized by an ability to bind with the cortisol receptor. Once diabetes was established, the researchers surgically removed the vagus nerve. The vagus nerve is the only nerve that starts in the brainstem and extends all the way down to the abdomen. More impressive is the fact that once the nerve was removed from the diabetic mice, insulin resistance and high blood pressure was prevented or reversed. This is an interesting discovery because people with asthma, arthritis, and organ transplants often rely on steroid treatments. It just so happens that many of them go on to develop insulin resistance.

Don't go ripping your vagus nerve out just yet. A fun fact about the vagus nerve is that it's name is taken from the Latin word meaning "wanderer". The vagal nerve pathway can influence seizures, depression and other disorders. Although the research is thoroughly enlightening, it is still very green. Hang on to your vagus nerve while the research continues.

Insulin, as incredible as it is in terms of its ability to help regulate blood sugar levels, may be worthy of even greater praise. That's because scientists (A.K.A. those smart people who went to a better college than I did) have discovered that applying insulin directly to wounds my actually help them heal more quickly.

Tests performed first on rats and then on human skin cells in culture resulted in the interesting discovery that wounds treated topically with insulin healed faster than wounds left untreated. The scientists examined the molecular impact of the topical application of insulin on keratinocytes, which are the cells responsible for regenerating the epidermis after wounding. The scientists also looked at microvasular endothelial cells, which are the cells that restore blood flow to a wounded area.

The evidence from these examination is what lead the scientists to their conclusions. Further, they speculated that this apparent link between insulin and healing may work to explain why many people with diabetes heal very slowly when wounded. Given the fact that people with diabetes suffer from impaired production or utilization of insulin, it stands to reason that this may be one of the reasons behind why healing may be impaired.

Diabetes Mine's Amy Tenderich is blogging the American Diabetes Association's 66th Annual Scientific Sessions. While Richard Kahn, Chief Scientific & Medical Officer for the American Diabetes Association is blogging the same convention, Tenderich promises to give her readers the uncensored and totally unofficial scoop. I believe she will more than deliver on her promise.

I am certain everyone in the online diabetes community is well aware that Tenderich blogs the Diabetes Mine, but if you are new to diabetes and reading this, her blog is a must visit. Amy -- diagnosed with Type 1 diabetes three years ago -- is all-things-real with the intelligence and sharp commentary to back it up. A most excellent blogger and blog.

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.