UM scientists create fruit fly model to help unravel genetics of huma...( College Park Md -- As rates of obes...)

College Park, Md -- As rates of obesity, diabetes, and related disorders have reached epidemic proportions in the US in recent years, scientists are working from many angles to pinpoint the causes and contributing factors involved in this public health crisis. While sedentary lifestyles and diets high in sugar and fat contribute significantly to the rise in diabetes rates, genetic factors may make some people more vulnerable than others to developing diabetes.

Researchers at the University of Maryland are using the fruit fly, Drosophila melanogaster, as a model system to unravel what genes and gene pathways are involved in the metabolic changes that lead to insulin resistance and full-blown diabetes in humans. In research published in the Proceedings of the National Academy of Sciences (November 2, 2009), Leslie Pick, associate professor, department of entomology, and colleagues describe how they altered genes in fruit flies to model the loss of insulin production, as seen in human Type 1 diabetes.

"These mutant flies show symptoms that look very similar to human diabetes," explains Dr. Pick. "They have the hallmark characteristic which is elevated blood sugar levels. They are also lethargic and appear to be breaking down their fat tissue to get energy, even while they are eating a situation in which normal animals would be storing fat, not breaking it down."

Pick and her team, which included UM researchers Dr. Hua Zhang, Dr. Jingnan Liu, and Ms. Caroline Li, Associate Professor Bahram Momen (Biostatistics and Environmental Science), and former Johns Hopkins University Associate Professor Dr. Ronald Kohanski, used genetic approaches to delete a cluster of five genes encoding insulin-like peptides (Drosophila insulin-like peptides, DILPs) in the Drosophila melanogaster fruit fly. "When we compare the mutants with a normal fly that has been starved, they look the same in that they are both breaking down
'/>"/>