Abstract
All forms of diabetes mellitus are characterized by chronic hyperglycemia and inflammation resulting in the development of numerous microvascular and macrovascular pathologies. Diabetes is also associated with changes in brain microvasculature leading to dysfunction and disruption of the blood–brain barrier (BBB). Despite the similarities between type I and type II diabetes, their effect on the BBB differ. In our streptozotocin (STZ)-induced model of type I diabetes where insulin and leptin levels are low, BBB disruption to 14C-sucrose occurred in the whole brain and specifically in the cortices, thalamus and midbrain after 16 weeks of induction. These mice also showed blood-retinal barrier (BRB) disruption. In our diet-induced obese model of type II diabetes where insulin and leptin levels are high, BBB disruption to 14C-sucrose was observed only in the hypothalamus and hippocampus after 16 weeks of high fat feeding. After 36 weeks of HF feeding, we observed BRB disruption in addition to hypothalamic and hippocampal disruption. Another model of type II diabetes is the BTBR ob/ob model, which is a transgenic model with no leptin production and high insulin. The BTBR ob/obmice show whole brain and retinal disruption to 14C-sucrose as early as 4 weeks of age. Understanding differences in these models is important in understanding the roles of insulin and leptin in BBB disruption.
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