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School of Medicine
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Sangwon Kim, Ph.D.
Associate Director of Endocrinology, Diabetes and Metabolism Research Laboratories
Associate Professor of Medicine
Research Interests: Obesity; Neuron; nutrient sensing; lipid; signal transduction; inositol pathway; an interaction between energy balance and neuronal function ...read more
Dr. Kim is an Associate Professor of Medicine and an Associate Director of Endocrinology, Diabetes and Metabolism (EDM) Research Laboratories.
Dr Kim’s laboratory studies how energy balance is sensed at the cellular level and how energy imbalance ultimately affects neuronal functions and behaviors.
Dr. Kim received his BS degree in biophysics with highest distinction at Iowa State University and PhD degree in Experimental Medicine with honor at McGill University, Montreal, Canada. He pursued his postdoctoral training at Department of Neuroscience Johns Hopkins University School of Medicine. Upon completion of his postgraduate training, he moved to Philadelphia as Assistant professor at Department of Psychiatry and Pharmacology, University of Pennsylvania School of Medicine.
Dr. Kim received The A. McGee Harvey Young Investigator Award (Johns Hopkins University School of Medicine), Pathway to Independence (NIMH), Intellectual and Developmental Disabilities Research Center Young Investigator Award (Children’s Hospital of Philadelphia), and National Alliance for Research on Schizophrenia and Depression Young Investigator Award.
- Associate Director of Endocrinology, Diabetes and Metabolism Research Laboratories
- Associate Professor of Medicine
- B.S., Iowa State University (Iowa) (1996)
- Ph.D., McGill University (Canada) (2002)
Johns Hopkins University School of Medicine, Solomon H Snyder Department of Neuroscience (2006)
Research & Publications
a) Nutrients (amino acid, glucose and lipid)-Mediated Signaling.
The ability to sense availability of nutrients and to regulate energy balance is fundamental process of all the living creatures. Obesity is an increasingly common health problem in the U.S. and throughout the developed world. Approximately two-thirds of the U.S population is currently obese or overweight. It has been acknowledged as the second leading cause of death, behind smoking. Obesity has been linked to diabetes, hypertension, cardiovascular disease, cancer, and a myriad of other health problems. Obesity results from disturbed energy balance, where energy intake (i.e. feeding) chronically exceeds total energy expenditure. Hence one of the key processes in the energy balance is to sense and respond to changes in nutrients (e.g amino acids, glucose, or lipid). A flurry of research activities has identified many genetic or biochemical components for nutrients sensing and has elucidated their roles in obesity and obesity-associated diseases. However the exact mechanism underlying development of obesity and interplay between numerous components are poorly understood. One of the primary goals in my laboratory is to understand how our body senses and responds to different levels of nutrients such as glucose or lipid, and how different pathways cross talk to each other.
b) Interaction between metabolic balance and neuronal function
Obesity is characterized by excessive accumulation of fat in adipose tissue as well as liver, muscle and other organs. Excess adiposity induces insulin resistance, which predisposes to diabetes when the pancreatic islets are unable to produce enough insulin to compensate for the increased metabolic demands of obesity. More than two-thirds of adults in the United States are overweight or obese, which increases the risk for diabetes, heart disease, stroke, some forms of cancer, and other health problems. Epidemiological studies find an association between Type II diabetes mellitus (T2D), cognitive impairments, and dementia including Alzheimer's disease (AD). The published work from Dr Kim’s lab established that sub-chronic HFD exposure leads to 1) neuronal insulin resistance, one of the hallmarks of metabolic syndrome, 2) reduced expression of synaptic markers, 3) a reduced long term potentiation and 4) reduced learning and memory function. Therefore, they are currently focusing their efforts on elucidating the molecular mechanism by which energy imbalance affects neuronal functions utilizing cellular and animal models.
Lab Website: Kim Lab
Brynildsen JK, Lee BG, Perron IJ, Jin S, Kim SF, and Blendy JA.:Activation of AMPK by metformin improves withdrawal signs precipitated by nicotine withdrawal.Proc Natl Acad Sci U S A. 2018 Apr 2. pii: 201707047. doi: 10.1073/pnas.1707047115. [Epub ahead of print]
Chen Y, Bang S, McMullen MF, Kazi H, Talbot K, Ho MX, Carlson G, Arnold SE, Ong WY, Kim SF: Neuronal activity induced sterol regulatory element binding protein-1 (SREBP) is disrupted in dysbindin null lice-Potential link to cognitive impairment in schizophrenia. Molecular Neurobiology. In Press 2016
Bang S, Chen Y, Ahima RS, Kim SF: Convergence of IPMK and LKB1/AMPK signaling pathways on metformin action. Molecular Endocrinology 28(7): 1186-1193, 2014
Arnold SE, Lucki I, Brookshire BR, Carlson GC, Browne CA, Kazi H, Bang S, Choi BR, Chen Y, McMullen MF, Kim SF: High fat diet produces brain insulin resistance, synaptodendritic abnormalities and altered behavior in mice. Neurobiology of Disease 67: 79-87, 2014
Bang S, Kim S, Dailey MJ, Chen Y, Moran TH, Snyder SH, Kim SF: AMP-activated protein kinase is physiologically regulated by inositol polyphosphate multikinase. The Proceedings of the National Academy of Sciences in the United States of America 109(2): 616-620, 2012
Contact for Research Inquiries
5501 Hopkins Bayview Cir
Asthma and Allergy Center, 2A44A
Baltimore, MD 21224 map