Gene discovered linking high-fat diet to diabetes
Key points
- A team at the University of California at San Diego has identified a gene that produces an enzyme that enables cells in the pancreas to recognize glucose and secrete insulin.
- In a study published in the research journal Cell, Dr.
- Marth's team studied mice that did not carry the GnT-4a gene and found that the animals initially had high blood glucose levels, which progressed to beta cell failure followed by the development of type 2 diabetes.
- Normal mice that carried the GnT-4a enzyme but were fed a high-fat diet had reduced GnT-4a expression, followed by the chain of events leading to type 2 diabetes.
A team at the University of California at San Diego has identified a gene that produces an enzyme that enables cells in the pancreas to recognize glucose and secrete insulin. Furthermore, a high fat diet suppresses the enzyme.
In a study published in the research journal Cell, Dr. Jamey D. Marth and colleagues describe the gene that encodes GnT-4a, a glucose transporter enzyme. Without GnT-4a, beta cells in the pancreas fail to produce insulin when exposed to glucose and fat.
Marth's team studied mice that did not carry the GnT-4a gene and found that the animals initially had high blood glucose levels, which progressed to beta cell failure followed by the development of type 2 diabetes.
Normal mice that carried the GnT-4a enzyme but were fed a high-fat diet had reduced GnT-4a expression, followed by the chain of events leading to type 2 diabetes.
"Our findings suggest that the current human epidemic in type 2 diabetes may be a result of GnT-4a enzyme deficiency," Marth commented in a university release.
If further research confirms the findings, one possible clinical application would be the development of therapeutic agents that boost GnT-4a levels, and Marth is currently working on this.
Agents that inhibit GnT-4a may also be useful in preventing a number of diseases inked to too much insulin production, such as cancer and cardiovascular disease.
SOURCE: Cell, December 29, 2005.
Written and revised by
David Cohen, M.D.
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