Our research focuses on the mechanisms by which skeletal muscle deals with the chronic oversupply of energy and the potential role such mechanisms may play in the development of metabolic diseases (i.e., obesity, insulin resistance, diabetes).
Our focus is on the mitochondria, the metabolic cellular engine. Under normal circumstances, the demand for energy by the cell sets the rate at which the engine (mitochondria) operate. However, when the supply of fuel (food) exceeds the needs of the cell, it is our hypothesis that this places what is known as reducing pressure (fuel overload) on the mitochondria. The build-up of pressure causes the mitochondria to leak electrons (i.e., release valve) to oxygen, generating hydrogen peroxide (H2O2). H2O2 in turn regulates the redox state or electrical charge throughout the cell.
Thus, the reducing pressure on the engine, the release valve, and the consequent regulation of the electrical charge are what we hypothesize are controlling insulin sensitivity in muscle. Research in my lab is directed at deciphering the molecular mechanisms governing mitochondrial bioenergetics and it's function in metabolic disease, it's treatment, and prevention.