New Research On Obesity and Insulin Resistance: While researchers know that it is obesity that leads to many cases of type 2 diabetes, researchers are partly stumped as to why excessive weight leads to insulin resistance and then to diabetes. At the Joslin Diabetes Center, scientists have found a new way in which obesity affects the body. They have found that in altering the production of proteins in which affects other proteins that are combined together.
The scientists began by examining levels of proteins in the livers of obese people in the lab of Mary-Elizabeth Patti, M.D., they’re findings consisted of a decrease in the number of certain proteins that regulate RNA splicing.
Dr. Patti, the Assistant Professor of Medicine at Harvard Medical School explains, “When a gene is transcribed by the cell, it generates a piece of RNA. That piece of RNA can be split up in different ways, generating proteins that have different functions.” Additionally, Dr. Patti stated, “In the case of these proteins whose production drops in the livers of obese people, this process changes the function of other proteins that can cause excess fat to be made in the liver. That excess fat is known to be a major contributor to insulin resistance.”
Through this study, researchers also showed that the RNA splicing proteins were decreased in the samples of the liver muscle from the obese people studied during their tests.
Through more research, the representative RNA-splicing protein called SFRS10 was examined. The SFRS10 levels dropped in muscle and liver in obese people and in over-fed mice as well. The tests showed that the SFRS10 helped to regulate the protein referred to as LPIN1, which plays a huge and important role in synthesizing fat. In their research of mice, researchers found that when they suppressed the production of SFRS10, more triglycerides developed which is a type of fat that circulates in blood.
Dr. Patti discusses the research further, “More broadly, this work adds a novel insight into how obesity may induce insulin resistance and diabetes risk by changing critical functions of cells, including splicing. This information should stimulate the search for other genes for which differences in splicing may contribute to risk for type 2 diabetes. Ultimately, we hope that modifying these pathways with nutritional or drug therapies could limit the adverse consequences of obesity.”
