UCSD FINDS PROTEIN THAT INDUCES DIABETES

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By Jaden Jimenez

June 18, 2014 (San Diego) -- Researchers at the University of California, San Diego School of Medicine have, for the first time, described the sequence of early cellular responses to a high-fat diet, one that can result in obesity-induced insulin resistance and diabetes.

Doctor Jerrold Olefsky, associate dean for Scientific Affairs and Distinguished Professor of Medicine at UC San Diego said, “We’ve described the etiology of obesity-related diabetes. We’ve pinpointed the steps, the way the whole thing happens,”

he also added, “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 and prevent it.”

Diabetes is the seventh leading cause of death in the United States and a major risk factor for other life-threatening conditions, including heart disease and stroke.

More than 25 million Americans have diabetes with another 79 million Americans estimated to be pre-diabetic, according to the American Diabetes Association.

Diabetes is characterized by high blood sugar levels poorly regulated by either inadequate insulin production or because cells do not respond properly to the regulating hormone.

Yun Sok Lee, PhD, a project scientist in doctor Olefsky’s lab, and colleagues fed mice a high-fat diet. They observed that the large amounts of saturated fatty acids in the diet activated ANT2, a protein in fat cells that is involved in energy metabolism.

Activation of ANT2 caused increased oxygen consumption, which meant less was available for the rest of the cell. This subsequently induced production of HIF-1alpha, a protein made to send signals of distress to the immune system causing an inflammatory response eventually leading to an insulin resistance in the cell.

The researchers suggest that inhibiting either ANT2 or HIF-1alpha could blunt, or even reverse, the damaging cellular sequence. Following that, they found that mice genetically engineered to lack HIF-1alpha in their fat cells were protected from high-fat diet-induced inflammation, insulin resistance and elevated glucose levels.

 


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