The researchers also report that knocking out a single gene encoding the enzyme GnT-4a glycosyltransferase (GnT-4a ) disrupts insulin production.
More importantly, the scientists using mice showed that a high-fat diet suppresses the activity of GnT-4a and leads to type 2 diabetes due to failure of the pancreatic beta cells.
The discovery of the link between diet and insulin production offers new information that may aid in the development of treatments that target the early stages of type 2 diabetes.
In the initial stages of the disease causes failure of insulin-secreting beta cells in the pancreas, which leads to elevated blood glucose levels. As the disease progresses, the insulin-secreting beta cells overcompensate for the elevated blood glucose, and eventually pump out too much insulin. This leads to insulin resistance and full-blown type 2 diabetes.
The new studies suggest that people with an inherited predisposition to type 2 diabetes may have discrepancies in a particular gene.
Jamey Marth, a Howard Hughes Medical Institute investigator at the University of California, San Diego says, "If our findings can be applied to humans, they should give us important insights into how type 2 diabetes may be prevented and treated."
While a deficiency of insulin can cause diabetes, too much insulin can also be harmful, and has been found to contribute to the pathogenesis of cancer, cardiovascular disease, ovarian diseases, and Alzheimer's disease.
Researchers calculate worldwide, more than 200 million people have type 2 diabetes, and close to 20 million people in the United States have been diagnosed with the disorder.
