Division of Endocrinology & Diabetes

Young-Hwan Jo, Ph.D.

Dr. Young-Hwan Jo

Assistant Professor, Department of Medicine (Endocrinology)

Assistant Professor, Department of Molecular Pharmacology


Professional Interests


Obesity is a chronic metabolic disorder characterized by an excess of body fat. Obesity results from prolonged positive energy balance (i.e. energy intake exceeding energy expenditure). Because obesity may develop over many years in humans, only small imbalances in energy intake and expenditure are required. The cause of excessive positive energy balance in obesity has not been clearly defined. Nevertheless, key regulatory components reside in the hypothalamus, specifically in the arcuate nucleus (ARC).

The central melanocortin system within the ARC is made up of two distinct subsets of neurons that express either pro-opiomelanocortin (POMC) or agouti-related peptide (AgRP). These peptides regulate their downstream target sites via modulation of melanocortin receptor type 3 (MC3R) and melanocortin receptor type 4 (MC4R) activity. Although POMC neurons were long considered to be a single homogeneous entity, recent studies, including our own, support considerable heterogeneity among POMC neurons. In particular, there are at least two phenotypically distinct populations of POMC neurons in the ARC. We hypothesize that these phenotypic distinctions reflect important functional differences and that the interplay between the phenotypically distinct populations of POMC neurons is required for integration of peripheral and central signaling molecules, thus controlling the anorexigenic outcome of POMC neurons. Thus we are currently determining how novel interactions between distinct populations of POMC neurons contribute to the control of hypothalamic neurophysiology and the regulation of energy homeostasis. Our laboratory employs optogenetics, electrophysiology and transgenic animal models to explore the physiological functions of these novel interactionsat the cellular and whole body levels. Understanding POMC-POMC neuronal interactions will help elucidate the elementary hypothalamic microcircuits controlling feeding and energy expenditure. Hence, this understanding will be crucial as we seek to determine the underlying cellular pathogenesis of the ongoing epidemic of obesity.


Selected Publications

Recent Publications (2009- present)

1. Leshan, R, Louis, G., Jo, YH, Rhodes, C., Munzberg, H. and Myers, M. Jr (2009) Direct innervation of GnRH neurons by metabolic- & sexual odorant-sensing leptin receptor neurons in the hypothalamic ventral premammillary nucleus. J. Neurosci., 29 (10): 3138-3147

2. Jo, YH*, Su, Y., Gutierrez-Juarez, R. and Chua, S.C. (2009) Oleic acid directly regulates POMC neuron excitability in thehypothalamus. J. Neurophysiol. May; 101(5):2305-16

3. Blouet, C., Jo, YH, Li, X. and Schwartz, G., (2009) Mediobasal hypothalamic leucine sensing regulates food intake through activation of a hypothalamic-brainstem circuit. J. Neurosci. Jul 1; 29(26):8302-11

4. Leinninger, GM, Jo, YH, Leshan, RL, Louis, GW, Yang, H, Barrera, JG, Wilson, H, Opland, DM, Faouzi, MA, Gong, Y, Jones, JC, Rhodes, CJ, Chua, S, Diano, S, Horvath, TL, Seeley, RJ, Becker, JB, Münzberg, H and Myers, MG (2009) Leptin Acts via Leptin Receptor-Expressing Lateral Hypothalamic Neurons to Modulate the Mesolimbic Dopamine System and Suppress Feeding. Cell Metabolism, Vol. 10 (2), 89-98

5. Chun, SK and Jo, YH* (2010) Loss of leptin receptors on hypothalamic POMC neurons alters synaptic inhibition J. Neurophysiol.Nov; 104 (5):2321-2328

6. Jo, YH*, Donier, E, Martinez, A, Garret, M, Toulmé, E, and Boué-Grabot, E* (2011) Crosstalk between P2X4 and GABAA receptors determines synaptic efficacy at central synapses J. Biol. Chem. June 3, 2011 Vol. 286. 19993-20004 *corresponding author

7. Leinninger, GM, Opland, DM, Jo, YH, Faouzi, M., Christensen, L., Yang, H., Becker, JB., Thompson, RC., and Myers, MG. Jr. (2011) Leptin action via neurotensinergic lateral hypothalamic neurons controls orexin, the mesolimbic dopamine system and energy balance. Cell Metabolism, Volume 14; 313-323

8. Jo, YH* (2012) Endogenous BDNF regulates inhibitory synaptic transmission in the ventromedial nucleus of the hypothalamus. J.Neurophysiol. Jan; 107: 42-49

9. Israel, DD, Sheffer-Babila, S, de Luca, C, Jo, YH, Liu, SM, Xia, Q, Spergel, D, Dun, SK, Dun, NJ and Chua, SC (2012), Effects of leptin and melanocortin signaling on pubertal development and reproduction. Endocrinology, May;153(5):2408-19

10. Blouet, C., Lui, SM, Jo, YH, Li, X. and Schwartz, G., (2012) TXNIP in Agrp Neurons Regulates Adiposity, Energy Expenditure, and Central Leptin Sensitivity. J. Neurosci. Jul 18; 32(29):9870-9877



1. Hugel S, Jo, Y.H. and Schlichter R. (2009) Synaptic co-release of ATP and GABA: functional characteristics, modulation and physiological implications: Book Title: Co-Existence and Co-Release of Classical Neurotransmitters, Chapter 11 (Springer Verlag)

2. Jo, Y.H. and Chua, SC (2009) Transcription Factors in the Development of Medial Hypothalamic Structures. AJP-Endocrinology and Metabolism, Sep; 297(3):E563-7

3. Jo, YH and Boue-Grabot, E (2011) Interplay between ionotropic receptors modulates inhibitory synaptic strength. Communicative & Integrative Biology Vol. 4(6): 706-709


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