UCSD Researchers Find Protein That Triggers Diabetes

Posted by Alexander Nguyen
Times of San Diego 

June 8, 2014

The origins and steps of obesity-related diabetes have been established for the first time, according to a significant set of findings just published by researchers at the UCSD School of Medicine.

The researchers concentrated on a protein, called ANT2, that they believe causes diabetes in fat people.

UCSD Skaggs School of Pharmacy & Pharmaceutical Sciences. Courtesy of UCSD News Center

“We’ve pinpointed the steps, the way the whole thing happens,” said Jerrold M. Olefsky, associate dean for Scientific Affairs and Distinguished Professor of Medicine at UCSD.

“The research is in mice, but the evidence suggests that the processes are comparable in humans and these findings are important to not just understanding how diabetes begins, but how better to treat it and prevent it.”

In a study published this weekend in the medical journal Cell, the UCSD researchers described a sequence that begins at the cellular level, as cells react to high-fat diets. These high-fat diets can then result in obesity- induced insulin resistance, and then diabetes.

Olefsky and others have previously shown that obesity is characterized by low-grade inflammation in fat tissue, and that this inflammation can become chronic and result in insulin resistance and diabetes. In their most recent findings, the scientists describe the earliest stages of the process which begin before obesity manifests itself.

The scientists began by feeding mice a high-fat diet. They noticed that the high levels of saturated fatty acids in the diet activated a protein in the fat cell membranes, which in turn caused increased oxygen consumption in the cells.

The increased oxygen consumption by the ANT2 protein left less oxygen for the rest of the cell.

Without an adequate oxygen supply, the cells go through a process that ultimately launches the immune system’s inflammatory response system. A sustained high-fat diet ensured that the process continued unimpeded, and that led to obesity, chronic tissue inflammation and insulin resistance in the mice.

The researches found that by controlling certain aspects of the process, they could protect the mice from inflammation, insulin resistance and elevated glucose levels that were caused by the high-fat diet.

The researches suggest that by impeding two specific steps in the sequence, they could blunt or even reverse the damaging cellular sequence.

— City News Service