Date of Award

Spring 2007

Project Type


Program or Major

Animal Science

Degree Name

Master of Science


Humans with diabetes mellitus are two to five times more likely to develop cardiovascular disease and do so at a much younger age than non-diabetics. This study utilized the Syrian F1B hamster, a model of human atherosclerosis, to: (1) determine whether one intraperitoneal injection of streptozotocin (STZ) could induce a diabetic-like hyperglycemic state, (2) compare the development of atherosclerotic lesions between non-treated (N), hyperglycemic (G), hyperlipidemic (L) and combined hyperlipidemic/hyperglycemic (L+G) hamsters, and (3) determine whether lesion development was accelerated due to plasma levels of glucose, triglycerides, total cholesterol, non-HDL-C, HDL-C, or lipid hydroperoxides, or by the TC/HDL-C or TG/HDL-C ratio or the expression of MDA or LOX-1 in the vascular wall of the hamster aortic arch. Plasma, and aortic arch and pancreatic tissue were collected and analyzed at 10 and 20 weeks.

Hamsters receiving one intraperitoneal injection of 40 mg/kg body weight of STZ had significantly elevated glucose levels compared to non-STZ injected hamsters. They also exhibited another characteristic of human diabetes, the atherogenic lipid triad characterized by hypertriglyceridemia, increased small dense LDL, and by week 20 decreased HDL-C levels. The lack of dependence on insulin, and its apparent continued secretion from the beta cells in the STZ treated hamsters appears to be reflective of human type II diabetes with the L+G hamster exhibiting the conditions of both insulin resistance and insulin impairment. The L+G hamsters also exhibited extremely accelerated atherosclerosis while the G only hamster exhibited no lesion development. Hyperglycemia and lipidemia alone independently induced MDA and LOX-1 expression. The combination of hyperglycemia/hyperlipidemia could potentially increase the expression of MDA and LOX-1 requiring further investigation to quantitate these levels. Atherogenesis appeared to be mainly associated with increased TC and non-HDL-C. While hyperglycemia alone does not appear to induce atherogenesis it may contribute to the acceleration of atherosclerosis when combined with elevated numbers of small dense LDL particles, with oxidation a major contributing factor to the formation of such particles. Our findings suggest that the L+G Syrian F1B hamster is a useful model for determining the mechanism(s) involved in the development of accelerated atherosclerosis under the conditions of hyperglycemia.