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Researchers at UCLA Health uncovered new information about the role inflammation plays in mitigating liver fibrosis, which is associated with metabolic-associated fatty liver disease (MAFLD), one of the most common diseases in the world affecting up to 40 percent of U.S. adults. While inflammation in the liver has long been considered a prerequisite to developing liver fibrosis, the scarring and thickening of tissue that can impair the liver’s ability to function, this new research suggests that reducing inflammation may not influence the extent of fibrosis. “Liver fibrosis is the critical feature that creates chronic liver disease and liver cancer. If we can keep fibrosis in check then we can meaningfully impact liver disease,” said Tamer Sallam, MD, PhD, corresponding author of the study and vice chair and associate professor in the Division of Cardiology, David Geffen School of Medicine at UCLA.

Dr. Nguyen, assistant clinical professor of medicine, was awarded a K08 Clinical Investigator Award from the National Institute of Diabetes and Digestive and Kidney Diseases. This five-year award of $853,000 supports Dr. Nguyen’s research on the “Role of a Novel Methyltransferase in Liver Lipid Metabolism.” His work aims to characterize how a methyltransferase regulates cellular cholesterol metabolism and contributes to the development of steatotic liver disease.

Researchers from the UCLA Health Jonsson Comprehensive Cancer Center and UCLA Liver Basic Research Center have received two grants totaling $9.1 million from the National Cancer Institute to advance liquid biopsy technologies for the early detection of cancer, which can significantly improve treatment outcomes and reduce the number of deaths caused by the disease. A liquid biopsy is a promising non-invasive medical test using a small volume of blood that gives scientists insight into the genetic makeup of tumors. By analyzing these components, researchers can gain valuable information about the genetic mutations, alterations and other molecular changes associated with the presence of cancer.

Dr. Benhammou, assistant clinical professor of medicine, was awarded a seed grant from the UCLA Health Jonsson Comprehensive Cancer Center and UCLA Jonsson Cancer Center Foundation for her project, The Impact of Statins on Immune Checkpoint Inhibitors for the Treatment of Hepatocellular Carcinoma. The cancer research project was funded in the amount of $49,562 and the award period is February 1, 2024 - January 31, 2025.

UCLA researchers found that fasting increases the splitting of mitochondria, which may have implications for metabolic and aging-related diseases. In the study published in June, scientists examined the livers of mice that had been starved and identified the activated proteins, said Nuria Martinez-Lopez, PhD, adjunct assistant professor, the paper’s first author. They found that proteins in the mTORC2 cellular signaling pathway – known to be related to cell growth and metabolism – were activated by fasting, she added. These proteins increased the splitting of the mitochondria during fasting, which might allow cells to more efficiently burn fatty acids to cope with starvation, said Rajat Singh, MD, MBBS, professor of medicine, the paper’s corresponding author. 

Dr. Sammy Saab, medical director of the Pfleger Liver Institute and medical director of the Adult Liver Transplant Program, commented in a NBC News story on a recently published analysis of data on 32,726 adults who participated in the National Health and Nutrition Examination Survey. The analysis showed that overall, NAFLD rose from 16% in 1988 to 37% in 2018. Among Mexican Americans, the rate of NAFLD rose from 36% in 1988 to 58% in 2018, an increase of 61%. Among African Americans, it rose from 11% in 1988 to 25% in 2018, a 127% increase. Among white Americans, the rate rose from 15% in 1988 to 35% in 2018, for a 133% increase. The new study was co-authored by Dr. Theodore Friedman, an endocrinologist and professor of medicine at both the Charles R. Drew University of Medicine and Science and the UCLA David Geffen School of Medicine.

A new study sheds light on how autophagy, the body’s process for removing damaged cell parts, when impaired, can play a role in causing heart failure. The research team led by Dr. E. Dale Abel, chair of the Department of Medicine at UCLA, and Dr. Quanjiang Zhang, adjunct assistant professor of medicine at UCLA, identified a signaling pathway that links autophagy to the control of cellular levels of a key coenzyme known as NAD+, which is found in all living cells and is central to how our metabolism works. Researchers say these findings may have implications for heart failure treatment.