Sangwon Kim, Ph.D.

Headshot of Sangwon Kim
  • Associate Director of Endocrinology, Diabetes and Metabolism Research Laboratories
  • Associate Professor of Medicine


Endocrinology, Diabetes and Metabolism, Metabolic Syndrome, Obesity more

Research Interests

Obesity; Neuron; nutrient sensing; lipid; signal transduction; inositol pathway; an interaction between energy balance and neuronal function more


Dr. Kim is an Associate Professor of Medicine and Neuroscience. Also, Dr. Kim is 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 the highest distinction at Iowa State University and a Ph.D. degree in Experimental Medicine with honors at McGill University, Montreal, Canada. He pursued his postdoctoral training at the Department of Neuroscience at Johns Hopkins University School of Medicine. Upon completion of his postgraduate training, he moved to Philadelphia as an Assistant professor at the 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), National Alliance for Research on Schizophrenia and Depression Young Investigator Award and Discovery Award. more


  • Associate Director of Endocrinology, Diabetes and Metabolism Research Laboratories
  • Associate Professor of Medicine
  • Associate Professor of Neuroscience

Departments / Divisions



  • B.S.; Iowa State University (Iowa) (1996)
  • Ph.D.; McGill University (Canada) (2002)

Additional Training

Johns Hopkins University School of Medicine, Solomon H Snyder Department of Neuroscience (2006)

Research & Publications

Research Summary

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

Selected Publications

Clark JM, Garvey WT, Niswender KD, Schmidt AM, Ahima RS, Aleman JO, Battarbee AN, Beckman J, Bennett WL, Brown NJ, Chandler-Laney P, Cox N, Goldberg IJ, Habegger KM, Harper LM, Hasty AH, Hidalgo BA, Kim SF, Locher JL, Luther JM, Maruthur NM, Miller ER, Sevick MA, Wells Q.:  Obesity and Overweight: Probing Causes, Consequences, and Novel Therapeutic Approaches Through the American Heart Association's Strategically Focused Research Network. J Am Heart Assoc. 2023 Feb 21: 12(4): e027693

Jung I, Tu-Sekine B, Jin S, Anokye-Danso F, Ahima RS, Brown TT, and Kim SF: Dolutegravir suppresses thermogenesis via disrupting UCP1 and mitochondrial functions in brown/beige adipocytes in preclinical models. (2022) J of Infect. Dis

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

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

Contact for Research Inquiries

5501 Hopkins Bayview Cir
Asthma and Allergy Center, 2A44A
Baltimore, MD 21224 map

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