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Scientists reveal mechanism behind high-fat, diabetes link.

As a ray of hope, comes the research that links high fat diet to Type 2 Diabetes and so can suggest ways to avoid it.

Cell journal featured the study which identifies a molecular link between the // consumption of fatty foods and the disruption of insulin production.

University of California, San Diego (UCSD) School of Medicine, scientist say that a single gene encoding the enzyme GnT-4a glycosyltransferase (GnT-4a) is key to enabling the beta cells in the pancreas to sense blood glucose levels and appropriately produce insulin. This enzyme is not able to act by a high-fat diet, resulting in pancreatic beta cell failure and eventually leading to type 2 diabetes.

Done in mice they found that mice lacking the GnT-4a gene had elevated blood glucose concentrations, indicating diabetes. The consequent failure of beta cells to normally secrete insulin resulted in the development of the disease.

According to the latest research, the key role of the GnT-4a enzyme is to maintain glucose transporters on the surface of the beta cells in the pancreas. Pancreatic glucose transporters are necessary at the beta cell surface to sense glucose levels in the blood.

Dr Jamey Marth, UCSD professor of cellular and molecular medicine said, “Our findings suggest that the current human epidemic in type 2 diabetes may be a result of GnT-4a enzyme deficiency. The GnT-4a enzyme is required to synthesize a glycan structure that holds the glucose transporter in place at the beta cell surface. The loss of this key transporter is directly linked to reduced GnT-4a protein glycosylation, a high-fat diet, and type 2 diabetes.”

According to Marth and his colleagues, their latest findings could lead to a new approach to the prevention of diabetes resulting from a high-fat diet. This could be a big step in preventing this lifestyle disease.


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