Edward Weiss, Ph.D., assistant professor of nutrition and dietetics at Doisy College of Health Sciences at Saint Louis University, looked at a relatively common version of a gene called FABP2, which is involved in the absorption of fat from food.

Those people with the variant gene processed fat differently than those who don't have it. They burned more fat, which may have hindered their ability to remove sugar from the blood stream and burn it. Diabetes is characterized by too much sugar in the blood.

"This study adds to what was previously known about this gene variant by showing that after consuming a very rich milkshake, people with the variant gene process the fat from the drink differently than other people," Weiss says.

That is not to say that half of U.S. residents are destined to get diabetes, he adds.

"While the variation of the gene appears to contribute to the diabetes risk, it does not cause diabetes by itself," Weiss says.

"Many other genes, some known and some unknown, are involved in a person's overall risk of developing diabetes. Those are things a person can't control. But there are risk factors for diabetes that a person can change -- lifestyle factors, such as diet and exercise."

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"We knew it was an important process for the cell, but until this study, we didn't know exactly why it was so important," Ibba said. "Other researchers have actually disrupted this process in mice, and found that it leads to neurodegenerative diseases resembling Alzheimer's and Parkinson's."

Ibba and his team face more challenges. They want to know precisely how cells correct for these mistakes, and knowing this may give them insight to neurological diseases.

"The key to efficient cell growth is to limit the level of mistakes to a tolerable amount," Ibba said. "In spite of all its checks and balances, a cell isn't perfect. Even though textbooks tell you that gene expression is flawless, this just isn't possible in real life.

"Ultimately “ and it's a long way off “ we hope to develop a way to therapeutically correct for these errors," he said. "If we understand how these diseases start, and it relates to mistakes in the mechanism we studied, then there may be a means to try and correct these mistakes."

Ibba conducted the study with Ohio State colleagues Jiqiang Ling, a graduate research associate in the Ohio State Biochemistry Program, and Herv?© Roy, a postdoctoral researcher in microbiology.

This study was supported by a grant from the National Science Foundation.

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