Biography 

Dr. Tseng is an Assistant Professor of Medicine in Harvard Medical School and a Principal Investigator in the Section on Integrative Physiology and Metabolism at Joslin Diabetes Center.  She received her doctorate in Developmental Biology and Cellular and Molecular Biology from the University of Wisconsin-Madison under the supervision of Dr. Linda Schuler.  She completed postdoctoral training in the laboratory of Dr. C. Ronald Kahn at Joslin Diabetes Center, Harvard Medical School.  Dr. Tseng was a recipient of the Individual National Research Service Award from the National Institute of Health and was an Eleanor and Miles Shore Scholar in Medicine at Harvard Medical School. 

Research Summary 

Obesity is an epidemic health problem worldwide, and is a significant risk factor for many human diseases, including diabetes, dyslipidemias, non-alcoholic fatty liver, gallstones, cardiovascular disease, Alzheimer’s disease and even some cancers.  Obesity develops when energy intake exceed energy expenditure.  Despite this simple nature, the maintenance of energy balance is complex.  The long-term research interest in Dr. Tseng’s lab is to understand the regulation of energy homeostasis and use it to develop potential therapeutic approaches for obesity and related diseases.  The current research projects in Dr. Tseng’s lab are focused around the following specific areas: 

1. Role of developmental signals in the determination of brown versus white adipose cell fate 

2. Identification and characterization of progenitor/stem cells that give rise to different adipose depots 

3. Integration of central and peripheral controls on whole body energy homeostasis 

Published 

1.Anatomical localization, gene expression profiling and functional characterization of adult human neck brown fat.Cypess AM etal.Tseng YH.Nat Med. 2013 May; 

2.Brown-fat paucity due to impaired BMP signalling induces compensatory browning of white fat.Schulz TJ etal. .Nature. 2013 Mar; Tseng YH

3.Brown adipose tissue regulates glucose homeostasis and insulin sensitivity. 

Stanford KI etal.Tseng YH, Goodyear LJ.J Clin Invest. 2013 Jan; 

4.Increased mitochondrial activity in BMP7-treated brown adipocytes, due to increased CPT1- and CD36-mediated fatty acid uptake.Townsend KL etal.Tseng YH. Antioxid Redox Signal. 2013 Jul; 

5.Intrinsic differences in adipocyte precursor cells from different white fat depots.Macotela Y etal.Tseng YH, Kahn CR.Diabetes. 2012 Jul; 

6.Bone morphogenetic protein 7 (BMP7) reverses obesity and regulates appetite through a central mTOR pathway.Townsend KL etal.Tseng YH.FASEB J. 2012 May; 

7.Brown adipose tissue: Recent insights into development, metabolic function and therapeutic potential.Townsend K, .Adipocyte. 2012 Jan; Tseng YH

8.Insulin/IGF-I regulation of necdin and brown adipocyte differentiation via CREB- and FoxO1-associated pathways.Cypess AM etal.Tseng YH.Endocrinology. 2011 Oct; 

9.Identification of inducible brown adipocyte progenitors residing in skeletal muscle and white fat.Schulz TJ etal.Tseng YH.Proc Natl Acad Sci U S A. 2011 Jan; 

10.Cross talk between insulin and bone morphogenetic protein signaling systems in brown adipogenesis.Zhang H etal.Tseng YH.Mol Cell Biol. 2010 Sep; 

11.Cellular bioenergetics as a target for obesity therapy.Tseng YH, Cypess AM, Kahn CR.Nat Rev Drug Discov. 2010 Jun; 

12.Insulin and insulin-like growth factor-1 receptors act as ligand-specific amplitude modulators of a common pathway regulating gene transcription.Boucher J, Tseng YH, Kahn CR.J Biol Chem. 2010 May ;