New Hypothesis for the Role of Oxidants in Type 2 Diabetes

Type 2 diabetes is widely thought to  result from the build-up of an excess of oxidants in the pancreatic cells which control our blood sugar levels. However, Dr James Watson – one half of the famous duo that solved the structure of DNA – has put forward a hypothesis proposing exactly the opposite;  a lack, rather than a surplus of oxidants could cause type 2 diabetes. He has also suggested that dementia, cardiovascular disease, and even some cancers may result from a similar disease mechanism.

In patients with type 2 diabetes, inflammation harms pancreatic cells, preventing them from regulating blood-sugar concentration.  The conventional view of type 2 diabetes states that excess oxidants stress cells and enhance inflammation. However, as exercise – a recommended, front-line treatment for the disorder – is associated with a significant increase in oxidant production, its therapeutic effects are somewhat paradoxical. This has led the Nobelist to suggest that low oxidant levels lead to cell damage, and call for more detailed research into exercise and its effects on the body.

Oxidants and antioxidants are both needed in cellular reactions. In the endoplasmic reticulum, where proteins are folded, oxidants like hydrogen peroxide (H202) are essential for making the chemical bonds that stabilise protein structure. These unfolded proteins are functionless, and may lead to the damage-induced inflammation thought to be behind type 2 diabetes.

The hypothesis was published in the high-profile medicine journal, The Lancet. In a quote from Dr Watson on the front cover, he attributes his being healthy enough to work, at age 85, to playing singles tennis. Further research into exercise, diabetes, and oxidants is needed to support this hypothesis. This research is hoped to be stimulated in a meeting with many scientists from across the world at Cold Spring Harbour in New York, where Watson works, later this year.

To see the original article, please visit: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(13)62365-X/fulltext