Scientists believe they have pinpointed why high-fat western diets lead to diabetes.
The reason is that an enzyme vital to the production of insulin is suppressed by fatty foods.
Experiments with mice showed that without enough of the enzyme, the pancreas no longer produces enough insulin to cope with rising blood sugar levels.
Insulin, released by the beta cells of the pancreas, enables glucose to be used as an energy source and regulates its level in the blood.
The number of people with diabetes has soared over the past decade with the majority suffering from type 2 diabetes, the most common form of the disease which is thought to be linked to lifestyle. Often type 2 diabetes is associated with insulin resistance, when the body ceases to react properly to insulin.
Diabetes can greatly increase the risk of a host of serious and potentially life-threatening conditions, including heart disease, stroke, nerve damage and damage to organs and eyes.
For many years scientists have known that fatty diets, obesity and type 2 diabetes are linked, but have not been able to explain why.
Now researchers at the University of California at San Diego said the answer appeared to be an enzyme called Gnt-4a glycosyltransferase (Gnt-4a).
The enzyme plays a key role in enabling pancreatic cells to sense blood glucose levels and produce appropriate levels of insulin.
Prof Jamey Marth, who led the research, said: "We have discovered a mechanistic explanation for beta cell failure in response to a high-fat diet and obesity, a molecular trigger which begins the chain of events leading from hyperglycaemia (high blood sugar) to insulin resistance and type 2 diabetes." The scientists found that mice lacking the Gnt-4a gene had elevated blood glucose concentrations. Eventually, they developed full-blown type 2 diabetes.
When normal mice were fed a high-fat diet, Gnt-4a activity was reduced, producing a similar outcome.
"Our findings suggest that the current human epidemic in type 2 diabetes may be a result of Gnt-4a enzyme deficiency," said Prof Marth.
- PA