Catherine Miney, a senior biomedical engineering major at the University of Florida, was recently accepted into the UF University Scholars Program. She is currently a student in a lab overseen by UF Department of Surgery faculty.
Miney’s work focuses on understanding the role a certain protein plays in blocking cellular destruction in patients with chronic non-alcoholic fatty liver disease, or NALFD.
She is working under the guidance of Jae-Sung Kim, PhD, an associate professor in the department of surgery, pharmacology and therapeutics, the Institute on Aging, and anatomy and cell biology. The causes of NAFLD remain largely unknown. People who have the condition are most likely middle-aged and overweight, and they also tend to have diabetes and high cholesterol.
The researchers believe that chronic NAFLD is linked autophagy dysfunction — a process where the body releases proteins that target excess fat deposits and defective or damaged parts of energy-producing cells known as mitochondria. Miney and her team believe that enhancing the production of a certain protein can facilitate liver cells to remove excess fat and to clear dysfunctional mitochondria.
In a mouse model, researchers are treating liver cells with palmitic acid to replicate the effects of NAFLD and analyzing changes in certain proteins over 24 hours. Specifically, the team is targeting the chronic form of the disease.
Miney found that fat intake to the liver affects mitochondria, and too much fat intake significantly changes the mitochondrial autophagy — or mitophagy — process, Kim said. The changes aren’t immediately after fat intake — it takes time.
Miney’s data suggest that one-time or occasional exposure to a high-fat diet “is not that detrimental to the mitochondria” or may not place a person at a higher risk for NAFLD, Kim noted. “Repeated or chronic exposure makes the mitochondria dysfunctional or defective.”
The long-term goal, Kim said, is to develop therapeutic strategies against NAFLD and its progression to liver cirrhosis and cancer.