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Hongxia Ren, Ph.D.

Assistant Professor of Pediatrics
Center for Diabetes and Metabolic Diseases

Education/Training:
B.S. Fudan University, Shanghai, China (2002)
Ph.D. University of Michigan, Ann Arbor, MI (2009)
Postdoctoral Training, Columbia University, New York, NY (2016)

Research Details:
The overarching goal of my research is to understand the molecular and genetic mechanisms of the neuroendocrine regulatory roles in feeding and glucose metabolism. My studies lie at the interface of neuroscience and metabolism, aiming 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.

Search for Dr. Ren on PubMed

Most Recent/Relevant Publications:

Article:

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, Lu TY, McGraw TE, Accili D. Anorexia and impaired glucose metabolism in mice with hypothalamic ablation of Glut4 neurons. Diabetes. 2015 Feb;64(2):405-17.

Ren H, Yan S, Zhang B, Lu TY, Arancio O, Accili D. Glut4 expression defines an insulin-sensitive hypothalamic neuronal population. Molecular Metabolism. 2014 Apr; 3(4): 452-459

Ren H*, Plum-Morschel L*, Gutierrez-Juarez R,  Lu TY, Kim-Muller KY, Heinrich G, Wardlaw S, Silver R, Accili D. Blunted Re-feeding Response And Increased Locomotor Activity In Mice Lacking FoxO1 In Synapsin-Cre-Expressing Neurons. Diabetes. 2013 Oct;62(10):3373-83  (* Co-first 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.

Lin HV*, Ren H*, Samuel VT, Lee HY, Lu TY, Shulman GI, Accili D  Diabetes in mice with selective impairment of insulin action in Glut4-expressing tissues. Diabetes. 2011 Mar; 60(3):700-709. (* Co-first author)

Jiao S, Ren H, Li Y, Zhou J, Duan C, Lu L Differential regulation of IGF-I and IGF-II gene expression in skeletal muscle cells. Mol Cell Biochem. 2013 Jan;373(1-2):107-113

Ren H, Accili D, and Duan C Hypoxia converts the myogenic action of insulin-like growth factors into mitogenic action by differentially regulating multiple signaling pathways. Proc Natl Acad Sci U S A. 2010 Mar 30; 107(13):5857-5862.

Ren H*, Yin P*, and Duan C IGFBP-5 regulates muscle cell differentiation by binding to IGF-II and switching on the IGF-II auto-regulation loop. J Cell Biol. 2008 Sep 8; 182(5): 979-991. (* Co-first author)

Review:

Duan C, Ren H, and Gao S Insulin-like growth factors (IGFs), IGF receptors, and IGF-binding proteins: roles in skeletal muscle growth and differentiation Gen Comp Endocrinol. 2010 Jul 1; 167(3):344-351

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