Diabetes is a disease that has a major economic impact on the US, with an estimated cost of $ 98 billion per year. It is of particularly high impact in the Native / Hispanic and African American communities. Diabetes is caused by an inability to produce or properly use insulin, resulting in hyperglycemia. The major health concern for diabetics is cardiovascular disease, particularly stroke, with diabetics having approximately 3 times higher probability of and mortality from stroke. One of the major factors in stroke progression and damage is brain edema formation. Brain edema during stroke has been linked to a large influx of ions into the brain, leading to water accumulation. Under normal conditions ion transport into the brain is tightly controlled by an interaction of the tight junctions and ion transporter of the blood central nervous system barriers (BCNSB). In diabetes, ion transport dysfunction has been reported in a number of organs. In animal models of stroke, infarct size and edema are increased in diabetics compared to non-diabetics. It is our hypothesis that during diabetes, both the tight junctions and ion transporters of the BCSNB are altered, resulting in a reduced ability to maintain ion homeostasis. During stroke this results in a larger influx of ions, leading to a more significant edema formation and thus more damage. We will test this hypothesis by investigating the effect of diabetes on BCNSB ion transporter and tight junction expression and function in control and diabetic animals. Our eventual goal is to gain a better understanding on the mechanisms involved in diabetic stroke damage, which will hopefully lead to better treatment paradigms
