Submission Date

8-2-2024

Document Type

Paper- Restricted to Campus Access

Department

Health & Exercise Physiology

Faculty Mentor

Stephen C. Kolwicz

Comments

Presented during the 26th Annual Summer Fellows Symposium, July 19, 2024 at Ursinus College.

Project Description

Fatty acids are an important energy source in long-duration endurance exercise. Mitochondrial uptake of fatty acids can be inhibited by malonyl-CoA, produced by the enzyme Acetyl CoA Carboxylase 2(ACC2). Therefore, ACC2 could be a cellular target to promote fatty acid metabolism and enhance exercise performance. In this study, mice with a systemic deletion of ACC2 (ACC-TKO) and control mice, were confirmed by genotyping before the study began. Male and female mice (n=29 in each group) were randomly assigned to voluntary wheel running or sedentary groups. Mice in the voluntary wheel running group were provided unlimited access to a running wheel in their home cage for six weeks. A data acquisition system connected to the running wheel monitored daily activity. Running wheel activity was recorded at 30-minute intervals during each twenty-four-hour period over the six weeks and reported as total distance, average velocity, and peak velocity. The body weights of the wheel-running mice were assessed weekly. At the end of six weeks, the heart, quadriceps, spleen, and adipose tissue were harvested from each mouse and weighed. Glucose, ketone bodies, cholesterol, and triglycerides were measured in the blood of all mice. In addition, triglyceride content was measured in the quadriceps muscle. The collected data was used to determine: 1) the effects of deletion of ACC2 on physical activity levels; 2) the impact of chronic physical activity in ACC2-TKO mice on body weight and adipose tissue mass; and 3) sex dimorphism with ACC2 deletion and/or physical activity.

Download

Restricted

Available to Ursinus community only.

Share

COinS