26336-Ren, Hongxia
Faculty

Hongxia Ren, PhD

Assistant Professor of Pediatrics

Bio

Hongxia Ren, PhD. is an Assistant Professor and a member of the Stark Neurosciences Research Institute, the Center for Diabetes and Metabolic Diseases and the Herman B Wells Center for Pediatrics Research at Indiana University School of Medicine. 

Dr. Ren graduated with B.S. degree in biology from Fudan University, Shanghai, China. She received her doctoral degree from University of Michigan, Ann Arbor, MI. Her dissertation is titled "Insulin-like growth factor (IGF) signaling during myogenesis". She completed her postdoctoral training with Dr. Accili with focus on diabetes and obesity research at the Diabetes Research Center (DRC) in Columbia University, New York, NY. Dr. Ren joined the faculty rank as an Assistant Professor at Indiana University School of Medicine in 2016. 

In 2016, Dr. Ren joined Indiana University School of Medicine with funding from a pretigious NIH K99/R00 pathway to independence award. In 2020, she was awarded an R01 from the National Institutes of Health/NIDDK to pursue her studies of metabolic fundtion of Gpr17 in the gasstrointestinal tract. 

As an independent investigator, Dr. Ren has received multiple career awards, including Showalter Scholar Award, and Outstanding Young Investigator and Early Career Development Awards from CSCTR, Early Investigators Award from Endocrine Society, and IU Trustees Teaching Award. Dr. Ren has provided professional services as a member on NIH study sections and a member (ECR) of the Journal of Biological Chemistry editorial borad.

Key Publications

Ren H*, Cook JR, Kon N, Accili D*. Gpr17 in AgRP neurons regulates feeding and sensitivity to insulin and leptin. Diabetes. 2015 Nov;64(11):3670-9 (Epub 2015 Jul 15). (* Co-corresponding author)

Ren H, Orozco IJ, Su Y, Suyama S, Gutiérrez-Juárez R, Horvath TL, Wardlaw SL, Plum L, Arancio O, Accili D  FoxO1 Target Gpr17 Activates AgRP Neurons to Regulate Food Intake. Cell. 2012 Jun;149(6):1314-1326.

Reilly AM, Zhou S, Panigrahi S, Yan S, Conley JM, Sheets PL, Wardlaw SL, Ren H*. Gpr17-deficiency in POMC neurons ameliorates the metabolic derangements caused by long-term high fat diet feeding. Nutrition and Diabetes. 2019 Oct; 9(1): 29-40 (*corresponding author) PMID: 31611548 https://www.nature.com/articles/s41387-019-0096-7

 

*Ren H, Vieira-de-Abreu A, Yan S, Reilly AM, Chan O, Accili D. Altered central nutrient sensing in mice lacking insulin receptors in Glut4-expressing neurons. Endocrinology. 2019 Sep; 160(9):2038-2048 (*Lead corresponding author) PMID: 31199472 https://academic.oup.com/endo/article/160/9/2038/5518335

Titles & Appointments

  • Assistant Professor of Pediatrics
  • Adjunct Assistant Professor of Anatomy, Cell Biology & Physiology
  • Education
    2016 POSTDOC Columbia University
    2009 PhD University of Michigan
    2002 BS Fudan University
  • Research

    The overarching goal of Dr. Ren’s research program is to understand the molecular and genetic mechanisms of homeostatic regulations critical for feeding and glucose metabolism. Dr. Ren and fellow lab members aim to elucidate the pathophysiology of metabolic and neurological diseases with a combination of cutting-edge neuroscience, cellular, molecular, and genetic methodologies. 


    Obesity is a major contributor to type 2 diabetes and cardiovascular disease. Finding novel and effective biochemical pathways to target organs and processes involved in the pathophysiology of these conditions has acquired new urgency. Feeding behavior and energy expenditure are under the control of the hypothalamus, where neuronal circuits integrate internal signals, sensing food absorption and energy storage, and sending signals to regulate energy expenditure. Disruption of these mechanisms in the central nervous system leads to metabolic disease. Moreover, brain regulates peripheral metabolism via autonomic nervous system. Therefore, the brain presents an attractive tissue to target for the development of novel therapies for diabetes and obesity.


    Current research programs in the lab involve investigating how central nervous system (CNS) communicates with peripheral tissues in order to maintain the metabolic homeostasis, such as profiling of hypothalamic neuronal populations, functional mapping of neural circuitry, and characterizing the neuronal signaling properties of G protein-coupled receptors (GPCRs). GPCRs have been proven to be the most successful class of druggable targets, being 30-50% of the target of all FDA approved medication in the market. We have generated genetic mouse models for the following studies with the aims for developing novel therapeutics for neurological and metabolic diseases.


    1) The function of central GPCR signaling in feeding and metabolic regulation.
    2) Investigate the novel neuronal mechanisms critical for the pathophysiology of type 2 diabetes.

     

  • Professional Organizations
    American Association for the Advancement of Science
    American Diabetes Association
    Endocrine Society
    Society for Neuroscience
  • Clinical Interests

    Dr. Ren's group is interested in metabolic and neurological defects.

  • Awards
    Org: NIH NIDDK
    Desc: Pathway to Independence Award
    Scope: National
    Date:
    Org: Columbia University
    Desc: Naomi Berrie Fellowship
    Scope: University
    Date:
    Org: American Diabetes Association
    Desc: ADA post-doctoral fellowship
    Scope: National
    Date:
    Org: Keystone symposia NID/NIDDK
    Desc: travel award
    Scope: International
    Date:
    Org:
    Desc: Showalter Scholar
    Scope:
    Date:
    Org: Central Society for Clinal and Translational Research
    Desc: Outstanding Young Investigator
    Scope:
    Date:
    Org: Central Society for Clinal and Translational Research
    Desc: Early Career Development Award
    Scope:
    Date:
    Org: Endocrine Society
    Desc: Early Investigators Award
    Scope:
    Date:
    Org: Indiana University
    Desc: Trustees Teaching Award
    Scope: University
    Date:
    Org: NIH NIDDK
    Desc: R01
    Scope: National
    Date:

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