Alan R. Saltiel, PhD

At its most basic level, diabetes is simply a failure to communicate. For reasons scientists don't understand, cells stop “hearing” signals from insulin telling them to take up or stop releasing glucose, the sugar cells use to generate energy. When the intricate communications network between insulin and cells breaks down, glucose builds up to abnormal levels in the bloodstream producing all the symptoms we know as diabetes.

Alan Saltiel Photo: Paul Thacker

Alan R. Saltiel, PhD, the John Jacob Abel Collegiate Professor of the Life Sciences, is trying to understand the insulin signaling pathway and learn how defects in signaling can trigger diabetes. The answer to the puzzle may be inside fat cells. Scientists used to think these cells were simply warehouses where the body stores excess fat. But now researchers know that fat cells produce hormones, which affect insulin's ability to communicate with cells.

With one-third of American adults now considered to be obese, it's no accident that rates of Type 2 diabetes are more than twice as high as they were 20 years ago. Something about having too much fat upsets the delicate balancing act between insulin and glucose that keeps cells healthy. Saltiel is determined to find out what it is.

Researchers in Saltiel's laboratory have discovered that the communications network within cells is even more complicated that they thought. They have identified previously unknown signaling pathways, genes and proteins that play important roles in the signaling process, and found that insulin's signals are routed to different compartments inside the cell, depending on the nature of the message.

Every discovery adds one more piece to the puzzle of the obesity-diabetes connection. The work is difficult and frustrating. But Saltiel is confident that understanding these cell signaling pathways will lead to new breakthroughs in the treatment and prevention of diabetes.

Learn more about this work at the Alan R. Saltiel Lab