Submission Date

7-19-2024

Document Type

Paper- Restricted to Campus Access

Department

Health & Exercise Physiology

Faculty Mentor

Stephen Kolwicz

Student Contributor

Namir Jeffries

Second Student Contributor

Paige Ponzo

Comments

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

Project Description

An imbalance of energy intake and output can lead to the development of obesity. When foods rich in fat are consumed, cells can store excessive amounts of fat in the form of triglycerides. This increased triglyceride storage may cause a detrimental impact on cells and lead to heart, muscle, and liver dysfunction. Acetyl CoA carboxylase 2 (Acc2) is an enzyme that produces malonyl CoA which inhibits the mitochondrial uptake of fatty acids. A deletion of Acc2 reduces malonyl CoA and decreases inhibition of carnitine palmitoyl transferase 1 (Cpt1), and thus increases mitochondrial fatty acid transport. Therefore, the goal of this project was to determine whether a systemic deletion of Acc2 (Acc2-TKO) will increase fatty acid oxidation and prevent lipid accumulation in mice fed a high-fat diet. Male control (n=13) and Acc2-TKO (n=10) mice were fed a high-fat diet (90% calories from fat) for 6 weeks. A group of control mice (n=7) were fed a standard chow diet for comparison. At the end of the dietary feeding period, hearts, livers, and quadriceps muscles were collected and weighed. Blood was also collected from all mice. Triglycerides were measured in the heart, liver, and quadriceps of all mice using colorimetric assays. Glucose, ketone bodies, cholesterol, and triglycerides were measured in the serum harvested from the mice. The results of the study will determine whether promoting cellular fatty acid oxidation via deletion of Acc2 is a potential treatment to prevent lipid accumulation in chronic dietary lipid overload conditions.

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