Molecular mechanisms of impaired glucose transport in insulin resistance

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Type 2 diabetes represents one of the major worldwide health challenges, with more than 400 million people diagnosed. Insulin resistance, a condition where the hormone insulin is no longer able to efficiently control blood glucose levels, is a primary risk factor for the development of type 2 diabetes. In addition, insulin resistance is also linked to a number of other chronic diseases including cardiovascular disease, some cancers and neurodegenerative disorders. Therefore, treatments to overcome insulin resistance would provide new therapeutic options for type 2 diabetes and could help reduce the burden of other insulin-resistance associated diseases.Insulin lowers blood glucose levels, in part, by increasing glucose transport into fat and muscle tissue where it can be utilised or stored. One of the underlying causes of insulin resistance is a defect in the transport of glucose from the blood into these tissues. The processes within fat and muscle cells that are required for insulin to increase glucose transport in healthy individuals is well known. However, is not known how or which of these processes are impaired in insulin resistance. The aim of my fellowship proposal is to address this gap in knowledge by leading studies to identify the reason that the transport of glucose into fat and muscle tissue is disrupted in insulin resistance. The longer-term goal of my work is to use this information to identify rational ways to combat insulin resistance. Improving or restoring glucose transport into fat and muscle tissues to treat insulin resistance will have two major implications for human health. Firstly, this will address a current gap in treatment options for type 2 diabetes since there are no current medications that directly target glucose transport. Secondly, since insulin resistance is now linked to a several other chronic diseases, new therapies to overcome insulin resistance may have significant implications beyond type 2 diabetes.