Ben B. Yaspelkis III received both his Ph.D. and M.A. from the University of Texas. Both degrees are in Kinesiology with a specialization in Exercise Science. He also has a Bachelor of Science in Sports Medicine from Pepperdine University.
Skeletal muscle insulin resistance and Type 2 diabetes mellitus have been shown to result from genetic origins as well as from environmental factors such as alterations in dietary composition and/or lack of physical activity. However, it has not been fully resolved exactly how impairments in skeletal muscle insulin signaling are manifested and if these defects are entirely reversible. It has been noted that a link may exist between obesity, chronic low-grade inflammation and skeletal muscle insulin resistance.
The Yaspelkis laboratory has reported that in the skeletal muscle of the high fat-fed rat (an “environmental” model of insulin resistance) that activation of inflammatory pathways appear to contribute to impairing insulin-stimulated activation of phosphatidylinositol 3-kinase (PI3-K) activity. Recently, the Yaspelkis laboratory has been evaluating the relationship between the inflammatory signaling cascades and PI3-K activation. A main hypothesis we have been pursuing is that increased inflammatory pathway activation results in decreased insulin-stimulated PI3-K activation in skeletal muscle, but insulin-stimulated PI3-K activation can be rescued if inflammatory pathway activation can be attenuated.