Electronic Thesis and Dissertation Repository

Thesis Format

Monograph

Degree

Master of Science

Program

Kinesiology

Supervisor

Melling, Jamie

Abstract

Individuals with Type I Diabetes Mellitus (T1DM) are at an increased risk for developing secondary complications which increases their risk of premature death. While the risk of secondary complications is reduced with intensive insulin treatment (IIT) and aerobic exercise (AE), both interventional strategies increase the risk of hypoglycemia. This study examined the effects of a 60-min bout of forced treadmill AE on hepatic and muscular blood glucose (BG) metabolism. Nineteen Sprague-Dawley rats were divided into two groups: Sedentary Control Rats (SC; n=5), and Sedentary T1DM rats (DSC); T1DM rats were subcategorized into Diabetic Pre-Exercise (DPRE; n=14) and Diabetic Post-Exercise (DPOST; n=7). The study was conducted over twelve weeks and upon completion the DPOST group underwent a 60-min bout of AE. Immediately following the experimental protocol both liver and muscle tissue were analyzed to measure BG, hepatic and muscular glycogen, and several liver and muscular regulatory enzymes (G6Pase, PEPCK, AKT). The DPOST rats had significantly lower hepatic glycogen when compared to the SC group but there was no difference when compared to the DPRE rats. G6Pase protein content was greater in the DPOST when compared to the SC group. Phosphorylated AKT (P-AKT) was greater in DPOST rats when compared with both SC and DPRE groups. However, no significant differences were found in PEPCK protein content in response to diabetes and exercise. These findings suggest that during AE in T1DM rats both gluconeogenesis and both hepatic and muscle glycogen is underutilized leading to a reliance on circulating BG to meet the increased metabolic demands during exercise.

Summary for Lay Audience

Type 1 diabetes mellitus (T1DM) is a result of the destruction of pancreatic beta cells which produce insulin. Most individuals with T1DM have an impaired ability to keep their blood sugars in a healthy range and require insulin supplementation and are thus at a higher risk for developing secondary complications such as cardiovascular disease. The two best ways to decrease the risk of developing secondary complications include exercise and intensive insulin treatment; however, both of these treatment strategies increase the risk of blood sugars dropping too low (<3.0 mM; hypoglycemia). To further understand the physiological pathways that contribute to this response during exercise this study examined several glucose-related metabolic pathways in the liver and muscle. In this study there were two groups: (1) sedentary control rats (SC) and (2) T1DM rats (DSC) which were subcategorized into pre-exercise (DPRE) and post-exercise groups (DPOST). Over twelve weeks, weekly blood sugars and body masses were measured and the DPOST group underwent a 60-min bout of AE. After completion of the experimental protocol, several enzymes (G6Pase, PEPCK, AKT) in both liver and muscle glycogen content were analyzed. Significant reductions in hepatic glycogen storage were observed between T1DM groups (DPRE, DPOST) and SC but no differences across groups were found in muscle glycogen storage. Significantly greater concentrations of G6Pase were observed in DPOST when compared with SC; while significantly greater proportions of phosphorylated AKT (P-AKT) were observed in DPOST when compared with both SC and DPRE. Additionally, no significant differences were found in PEPCK protein content between the groups. These findings suggest that during AE in T1DM rats gluconeogenesis and both muscle and liver glycogen are underutilized, leading to a reliance on circulating blood sugar to meet the demands of exercise.

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