Myers, Martin G.
Molecular and neural mechanisms of leptin action
General Research Subject: Obesity
Focus: Integrated Physiology\Regulation of Food Intake, Obesity\Animal Models, Signal Transduction (Non-Insulin Action)\Transgenic Models
Type of Grant: Mentor Based Postdoctoral Fellowship
Project Start Date: July 1, 2011
Project End Date: June 30, 2015
This ADA mentor-based postdoctoral fellowship application focuses on shaping enthusiastic, skillful, creative researchers of high integrity under the mentorship of Martin Myers, MD, PhD. This is accomplished via diabetes-, metabolism-, and obesity-centered research training focused on leptin action. Leptin is a fat-derived hormone that controls body weight and blood sugar; alterations in leptin action are associated with obesity and type 2 diabetes. Research training in the Myers laboratory provides experience with important topics and techniques in diabetes research. As well as interacting with the mentor and others in the laboratory on a daily basis, the fellow will interact and collaborate with other investigators and researchers at the University of Michigan and worldwide through a variety of formal and informal mechanisms. In the laboratory, the fellow will employ a wide range of cutting-edge techniques to answer important biologic questions central to the mission of the ADA. The fellow will study cellular signals by which leptin regulates glucose homeostasis in animals. Exposure of the fellow to a broad diversity of researchers and methods within and outside of the Myers lab will empower this young researcher to engage new questions and develop novel solutions to biological problems related to obesity and diabetes.
Mentor: Myers, Martin, Jr., MD, PhD Postdoctoral Fellow: Patterson, Christa
What area of diabetes research does your project cover? What role will this particular project play in preventing, treating and/or curing diabetes?
This project deals with the basic mechanisms by which signals leptin act in the brain to control eating and glucose homeostasis- important for obesity and type 2 diabetes ('diabesity'). The central hypothesis of the grant is that the appetite-suppressing hormone, leptin, acts in part via STAT5 signaling to control glucose homeostasis, and also that novel and crucial sets of neurons in the brain. We will investigate STAT5 signaling and characterize the neurobiology and function of novel leptin-responsive neurons. If the data that we generate in this project support this theory, then we will have taken several steps toward characterizing potential therapeutic targets for the treatment of 'diabesity.'
This project will delineate the role for STAT5 in leptin action and in the control of glucose homeostasis, as well as investigating the function of important brain neurons that we believe acts to regulate feeding, feeding-related behavior, and metabolism. We hope that if our theories about these mechanisms prove to be correct, we will also gain some understanding of how they can be regulated to control appetite and that would work both as therapy for and prevention of obesity and Type 2 diabetes.
Why is it important for you, personally, to become involved in diabetes research?
On a personal note, Type 2 diabetes runs in my family, so that I have a personal as well as professional stake in the research. At a professional level, we are exposed to the horrors of diabetes on a daily basis in the Endocrinology and Diabetes Division at the University of Michigan; it seems incredible that medicine could have advanced so far in the past century and yet the incidence and prevalence of Type 2 diabetes continue to increase in the face of limited therapies. We find ourselves at an important juncture, however, where our knowledge is increasing logarithmically and improved prevention and therapy is likely to be rapidly forthcoming.
What role will this award play in your research efforts?
This award will enable us to carry forward projects that are a critical piece of my laboratory's overall effort toward a more global understanding of leptin and central mechanisms that regulate eating and glucose homeostasis. Without this award, we would not be able to undertake important aspects of these projects. I hope that these projects will provide not only information that is critical to this pursuit, but also open up new avenues for research that will enable us to obtain future NIH funding for subsequent projects.
In what direction do you see the future of diabetes research going?
Over the next few years, diabetes research will likely rely heavily on basic cell biology, the results of which will be translated into genetically engineered mouse models for initial testing and validation. Processes found to be important to these criteria will then move forward to testing in humans and for the development of therapeutic interventions.
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