Date of Award


Degree Name

Master of Science


Food and Nutrition

First Advisor

Banz, William


Hyperglycemia associated with diabetes has been recognized for adverse neurodegenerative effects it has on the central nervous system (CNS). However, few cerebral histopathological studies have been completed to adequately define the neuropathology of type 2 diabetes. The aim of the study was to conduct a neuropathological survey of diabetic Zucker Diabetic Sprague Dawley (ZDSD) rat brains that included a wide variety of potential pathologies. Ten ZDSD rat brains (diabetic: n=6 non-diabetic obese: n=4) were collected for neuropathological assessments. Specific measures include assessments of gray and white matter atrophy, neurodegeneration, astrocyte activation, blood brain barrier integrity, inflammation, and amyloid protein deposit. After brain sectioning, formal thionin, immunoglobulin G (IgG), glial fibrillary acidic protein (GFAP), giemsa, congo-red, and flourojade (FJ) stains were performed for analysis. Of the several neuropathological assessments, two revealed significant differences between diabetic and non-diabetic groups. Diabetic ZDSD rats had a relative decrease in the amount of white matter in the corpus callosum underlying the cingulate cortex of the brain. Secondly, higher numbers of lymphocytes were observed in the hypothalamus of the diabetic rats compared to non-diabetic rats. Enhanced expression of GFAP was not present. No measurable differences were observed in analysis of amyloid, FJ intensity levels or immunoglobulin G (IgG) extravisation into the brain. These results suggested that ZDSD rats do not exhibit neuropathology excepting white matter atrophy and increased lymphocyte infiltration into the hypothalamus, or that the duration of 6-7 month old diabetic ZDSD rats may be insufficient to support most of our hypotheses. Future work is required to determine profiles of neuropathology in longer term of diabetic ZDSD rats.




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