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Lei Wei, PhD

E-mail:renh@iu.edu
Phone: 317-274-1567
Office: MS2049

Hongxia Ren, PhD

Assistant Professor of Pediatrics

Primary Appointment: Department of Pediatrics, Wells Center for Pediatric Research

Member: Stark Neurosciences Research Institute

Education

  • B.S.: Life Science Institute (2002), Fudan University, Shanghai, China
  • PhD: Department of Medicine, Columbia University, New York, NY
  • Postdoctoral Fellowship Department of Medicine, Columbia University, New York, NY

Awards, Honors and Distinguished Professional Activities

  • NIH/NIDDK Pathway to Independence Award K99/R00
  • American Diabetes Association mentor-based post-doctoral fellowship
  • Naomi Berrie Fellowship in Diabetes Research Award
  • Keystone Symposia (Obesity) NIH/NIDDK travel grant
  • Marija Dokmanovic-Chouinard Award for Excellence in Research
  • Keystone Symposia (Diabetes) NIH/NIDDK travel grant
  • Gordon Research Conference travel grant
  • University of Michigan Rackham Graduate Student Research Grant
  • The 3rd International Congress of the GRS and the IGF Society travel grant
  • Chun-Tsung Scholarship for Undergraduate Scientific Research (2002)

Current Research Interests:

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.