Yu-Hua Tseng, PhD
Harvard Medical School
Dr. Tseng is a Principal Investigator in the Section on Integrative Physiology and Metabolism at Joslin Diabetes Center as well as an Associate Professor of Medicine at Harvard Medical School. She received her doctorate in Developmental Biology and Cellular and Molecular Biology from the University of Wisconsin at Madison and completed postdoctoral training in the Section on Cellular and Molecular Physiology at Joslin under C. Ronald Kahn, M.D. Dr. Tseng was a recipient of the Individual National Research Service Award from the National Institutes of Health and was a 2005 Eleanor and Miles Shore Scholar in Medicine at Harvard Medical School.
Obesity is an epidemic health problem worldwide, which results from an imbalance between energy intake and energy expenditure. Adipose tissue plays an important role in obesity, insulin resistance and diabetes. Two functionally different types of fat are present in mammals: white adipose tissue, which is the primary site of energy storage, and brown adipose tissue, which is specific to thermogenic energy expenditure. Yu-Hua Tseng, Ph.D., investigates factors that underlie the divergent differentiation fates and functions of these two adipose cell types. Given its specialized function to dissipate chemical energy, brown adipose tissue provides a natural defense against cold and obesity.
Several developmental signaling molecules have been shown to impact the development of different adipose depots. Combining cellular, molecular and physiological approaches, Dr. Tseng and her colleagues have discovered that bone morphogenetic protein (BMP) 7 specifically promotes brown adipocyte differentiation and function. Treatment of mice with BMP7 results in an increase in brown fat mass and reduced weight gain. Current ongoing studies in Dr. Tseng’s lab aim to further determine the role of BMPs in the control of brown versus white adipogenesis and whole body energy metabolism using a variety of in vitro and in vivo approaches. In addition to BMPs, Dr. Tseng and her colleagues continue to identify additional factors that differentially regulate the development and function of brown versus white adipose tissue using genomics, proteomics, and small molecule screenings.
The adipose tissue arises from the multipotent stem cells of mesodermal origin. When triggered by appropriate developmental cues, these cells become committed to the adipocyte lineage. It has been suggested that different fat depots located in different anatomical locations of the body may derive from distinct developmental origins. Recently, Dr. Tseng and her colleagues have identified and isolated a subpopulation of adipogenic progenitors residing in murine brown fat, white fat, and skeletal muscle. Importantly, while the adipose progenitors from interscapular BAT are constitutively committed brown fat progenitors, precursor cells from skeletal muscle and subcutaneous white fat are highly inducible to differentiate into brown-like adipocytes upon stimulations, such as BMP7. Because of their inducible nature, these inducible brown fat progenitors hold great potential for developing new therapies for obesity by generating energy-expending brown fat cells using pharmacological or cell-based approaches.