Insulin signaling and associated pathways form a network that integrates information from diverse signals such as nutrition, growth hormones, and oxidative stress, and regulates cell growth, division, and death. Defects in this signaling network result in diseases such as diabetes, obesity, and cancer; nevertheless, little is known about how a cell integrates multiple inputs to choose between alternative outputs.
I am expanding a model of insulin signaling by Sedaghat et al. (2002) to include the known mechanisms by which excess lipids and amino acids downregulate the sensitivity of glucose transporters to insulin and regulate growth. Studying the dynamics of this network will help us understand the etiology of lipid- and amino-acid-induced insulin resistance.