Mitochondrial signaling in adipose tissue

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Obesity has become a significant health care concern globally. While a great deal of attention is being devoted to managing this condition, relatively little attention is devoted to understanding the biochemical origins of obesity. As the body begins to accumulate excess calories in the form of fat, the nature of the biochemical signals that dictate the balance between health and disease change. It is important to understand the significance of these changes. One of the major sources of these signals is fat or adipose tissue. Adipose tissue releases molecules, called adipokines, which communicate with a number of tissues throughout the body including the pancreas and heart. Some of these molecules cause inflammation and some may be responsible for causing type II diabetes. The important question that will be addressed in this research is "what properties of adipose tissue cause it to release these molecules?" We believe the fat senses metabolic stress from its mitochondria, the components of the cell that produce energy, and uses free radicals (produced by the mitochondria) as a means to signal the release of these adipokines. We will try to prove this by altering the level free radicals produced by fat cell mitochondria and determining the effect on the release of these signaling molecules.