Hope for four million Brits suffering from common condition after landmark study

Some of the mechanisms that trigger type 2 diabetes remain a mystery despite the major strides scientists have made with the disease in recent years.

But an international DNA study involving Cambridge University may now pave the way for further treatments for the condition that affects four million people in the UK and at least 460 million people worldwide. Several factors contribute to an increased risk of type 2 diabetes, such as older age, being overweight or having obesity, physical inactivity and genetic predisposition.

If untreated, type 2 diabetes can lead to complications including eye and foot problems, nerve damage and a raised risk of heart attack and stroke. Insulin, a hormone that regulates blood sugar – glucose – levels plays a pivotal role.

People who have type 2 diabetes are unable to correctly regulate their glucose levels. That can be because they don’t produce enough insulin when glucose levels increase, for example after eating a meal.

Or it can be because their cells are less sensitive to insulin, a phenomenon known as insulin resistance, and this plays a key role in the development of type 2 diabetes, but we don’t know the mechanisms at play. Insulin resistance can be shown up with a glucose challenge test – such as consuming a sugary drink after a meal – after which glucose levels in the body are tracked.

To examine these mechanisms, an international team of scientists used genetic data from 28 studies, encompassing more than 55,000 participants (none of whom had type 2 diabetes), to look for key genetic variants that influenced insulin levels measured two hours after consuming a sugary drink.

Ten new loci (regions of the genome, which are the complete set of DNA of an organism) were identified linked to insulin resistance after the sugary drink and were found to carry a higher risk of type 2 diabetes. One of these new loci was located within a gene named GLUT4 – responsible for moving glucose into fat and muscle cells. This locus caused GLUT4 to be less active in the muscle cells.

Experiments showed when less GLUT4 made its way onto the surface of a cell, the cell’s ability to remove glucose from the blood was impaired. Professor Claudia Langenberg, of Queen Mary University of London and the Berlin Institute of Health, Germany, said: “Our ­findings open up a potential new avenue for the development of treatments to stop the progress of type 2 diabetes.

“It also shows how genetic studies of dynamic challenge tests can provide important insights that would otherwise remain hidden.”