Study Links B-cells in Fat Tissue to Impaired Metabolism in Older Adults
Author: | June 26, 2020
Many of us have heard the saying, “An apple a day will keep the doctor away.” However, we know that health is much more complex than this. Research shows that our bodies are more susceptible to metabolic dysfunction as we age and that this dysfunction causes higher rates of certain diseases like diabetes among older individuals. But, research has yet to determine why the ability to break down fat is impaired by aging—it has yet to unravel this complexity. Or, it did.
New research published by Christina Camell, PhD, an assistant professor in the Department of Biochemistry, Molecular Biology and Biophysics at the University of Minnesota Medical School and College of Biological Sciences, in the journal, Cell Metabolism, reveals why visceral fat—fat stored in the abdominal cavity—increases with age and points to new treatment possibilities for improving metabolic health.
The study, which was conducted during Dr. Camell’s post-doctoral research at Yale University with Vishwa Deep Dixit, MD, used mouse models to demonstrate that cells found in the immune system, specifically B-cells, impair the metabolism of older-aged individuals. This causes increased inflammation and risk of metabolic and age-related chronic diseases. After discovering that B-cells existed en masse in fat tissue, the researchers found they could restore the body’s ability to burn fat and decrease inflammation by reducing B-cells in adipose (or fat) tissue.
“Finding that the frequency of B-cells are expanded in adipose tissue was unexpected,” Dr. Camell said. “But, overall, I think it’s important to identify these pathways or factors so that we can appropriately, maybe, intervene to block their contributions to metabolic dysfunction.”
Dr. Camell is currently working in her own lab at the U of M and conducting research with the U of M’s Institute on the Biology of Aging and Metabolism (iBAM) on the role of immune cells in tissue and the extent of their ability to affect metabolic dysfunction in elderly individuals. Since the start of the COVID-19 pandemic, Dr. Camell’s research has expanded to study how immune cells may contribute to COVID-19 morbidity in the elderly as well.
While the research is specific to mouse models for now, Dr. Camell hopes this will improve understanding— and the quality of life for aging individuals—sometime in the near future. “One of the cool things for me about aging research, and especially metabolic research, is that it is relevant,” Dr. Camell said. “We’re making it relevant so the general public can live a better quality of life, translating the research that we’re doing in mouse models to humans down the road.”