M-SURE Faculty Mentors

Christian R. Burgess, Ph.D. is an Assistant Professor in the Molecular & Integrative Physiology Department and the Michigan Neuroscience Institute. His lab studies the neural circuitry underlying feeding and food seeking behaviors, with a particular focus on learning and processing of food-related sensory stimuli. Much of human overconsumption of food, which can lead to obesity, is not due to homeostatic drive, but rather due to non-homeostatic factors, such as hedonic value, circadian factors, or the abundance of tempting food cues in our environment. Ongoing areas of study in the Burgess laboratory include: 1) Characterizing the role of MCH neurons in the lateral hypothalamus in homeostatic and non-homeostatic feeding behaviors, 2) Using in vivo two-photon imaging to elucidate how the brain processes food-related sensory stimuli, 3) investigating interactions between lateral hypothalamic peptidergic neurons and the limbic system during learning of food cues and acquisition/consumption of food.

Prof Coronel is a Biological scholar and Assistant Professor of Biomedical Engineering at the University of Michigan. Her lab is centered on engineering biomaterials for perturbing and investigating immunological responses. Dr. Coronel received her BS degree in Biomedical Engineering from the University of Miami, and her Ph.D. in Biomedical Engineering from the University of Florida. She also obtained a certificate in Clinical Translational Research from Emory University Public Health School. She finished her postdoctoral fellowship at the Georgia Institute of Technology, where she received funding from the Juvenile Diabetes Research Foundation, NIH T31, and Georgia CTSA to support her training. CV.

Carrie Ferrario, PhD is an Associate Professor in the Department of Pharmacology at the University of Michigan. Her lab studies how alterations in glutamatergic transmission within the striatum contribute to the development and persistence of obesity and drug addiction. Their long-term goal is to understand how sugary, fatty foods and physiological changes accompanying obesity alter brain function and behavior, how individual susceptibility to obesity interacts with these effects, and how mechanisms underlying strong urges to eat may compare to those that drive abuse of addictive substances like cocaine.

Kathy Gallagher, M.D. is an associate professor of Surgery. As a clinician-scientist, she has a long-standing defined clinical and translational interest in translational therapy to target inflammation in chronic wounds. Her long-term goal is to uncover the basic mechanisms responsible for the coordination of immune cells in early tissue repair processes, determine impairments in Type 2 Diabetes and translate this knowledge to the bedside. She has taken an active role in mentoring undergraduate and graduate students as well as post-doctoral fellows and residents and will continue to do so in my role on this R25. As is evident by my past and current trainees, I am committed to increase diversity, equity and inclusion in the scientific workforce and I have taken numerous workshops on unconscious bias, stereotype threat and leadership development. As surgeon-scientists are very underrepresented in science and our numbers continue to decline, I am committed to mentoring and training the next generation of surgeon-scientists. I feel qualified to be a mentor on the R25 grant “Michigan Summer Undergraduate Research Experience: Diabetes & Metabolic Diseases.” given my track record of training.

Brigid Gregg, MD is an Assistant Professor of Pediatrics in the Division of Endocrinology, Diabetes and Metabolism at Michigan Medicine. She is also an Assistant Professor in the Department of Nutritional Sciences at the University of Michigan School of Public Health. Dr. Gregg’s lab focuses on characterizing early life events that predispose individuals to developing metabolic disease, with the ultimate aim of identifying interventions to improve metabolic outcomes in high risk individuals. Dr. Gregg’s lab uses animal models along with a human mother infant cohort to study how nutritional influences very early in life can have a on body composition, adiposity, insulin sensitivity, glucose homeostasis, and pancreatic beta-cell mass and function. This translational approach is focused on exposures during the lactation period and the lasting impact these can have on offspring health.

Ken Inoki, M.D., Ph.D. is an associate professor of Molecular and Integrative Physiology and Internal Medicine, and a research associate professor in the Life Sciences Institute, University of Michigan. His research is focused on understanding the roles of nutrient-sensing machinery for cell growth/proliferation control and the development of metabolic disorders, such as diabetes and its complications. Using biochemical and cell-based biological approaches, he investigates novel proteins and their signal transductions that impinge on the mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) pathways. By generating various mouse models, his team characterizes the role of those novel signal transductions in the development of obesity and diabetic complications. He collaborates with many researchers in the field of diabetic and cancer research to identify potent and feasible therapeutic targets within those nutrient-sensing pathways.

Carey Lumeng, MD, PhD is a Professor of Pediatrics, Division of Pediatric Pulmonology, and Molecular & Integrative Physiology. His research centers on understanding the mechanisms by which obesity negatively impacts health. They strive to understand link between obesity and disease to enable the design of novel strategies to disrupt these connections. He has focused on understanding how the innate and adaptive immune system respond to dietary excess and contribute to metabolic dysfunction such as insulin resistance that are major risk factors for cardiovascular disease. Current projects in the lab focus on numerous aspects of adipose tissue immune network in health and disease. Projects focus on the regulation of adipose tissue macrophages in obesity and understanding how macrophage proliferation contributes to their regulation and polarization state. Translational research studies have identified novel genetic pathways relevant to metabolically unhealthy obesity phenotypes by collaborations with bariatric surgery to obtain omental and subcutaneous adipose samples. Recent efforts in the lab are using single cell and nuclear RNA sequencing approaches to delineate cellular diversity in adipose tissue in humans and mice in a team science approach with surgeons, bioinformaticians, and biologists.

Martin Myers, MD, PhD is Director, Michigan Diabetes Center (MDiabetes)/Elizabeth Weiser Caswell Diabetes Institute, and Professor of Internal Medicine (MEND) and Molecular & Integrative Physiology. His laboratory studies the molecular and neural mechanisms by which the brain controls metabolism, energy balance, and physiology. These studies are central to understanding mechanisms that may contribute to obesity pathogenesis. Major themes for the lab include the mechanisms and function of leptin receptor (LepRb) action, including downstream signals mediated by LepRb, as well as the neural mediators of leptin action (i.e., LepRb-expressing cells in the brain). To date, they have identified and demonstrated the functions for individual LepRb signals, revealing the central role for STAT3-dependent transcriptional control (as well as other signals) to leptin action. The Myers lab has revealed the importance of leptin action in the brain, including how LHA LepRb neurons that control the mesolimbic dopamine (reward) system and other hypothalamic neurons crucial for energy balance and the control of the hypothalamic melanocortin system. Recent snRNA-seq data have revealed novel populations of hypothalamic LepRb neurons that play crucial roles in energy balance and endocrine function.

Young Ah Seo, Ph.D. is an Assistant Professor in the Nutritional Sciences Department in the School of Public Health. Her research program has focused on new roles of metal ion transporters that are mutated in a variety of traits and diseases, including intestinal, metabolic, and neurological disorders. To define the roles of the mutated metal-ion transporters in related diseases, her research group employs novel combinatorial approaches, comprising the reverse genetics and phenotyping of mice, primary organoid cultures derived from genetically engineered mice, cell culture models of neuronal development, and functional genomics utilizing next-generation sequencing. Ongoing areas of study in the Seo laboratory include: 1) examining new roles of manganese in gut and metabolic disorders, 2) dissecting brain disorders associated with manganese misregulation, 3) mechanisms of brain iron overload and neurodegeneration with brain iron accumulation (NBIA), and 4) developing new approaches for treatment of human disorders of metal imbalance. Her research will provide the mechanistic basis upon which evidence-based therapeutics can be developed in the future.

Yatrik Shah PhD is a Professor of Molecular & Integrative Physiology and Internal Medicine, Division of Gastroenterology. Dr. Shah’s research focuses on determining the molecular mechanisms by which oxygen sensing transcription factors regulate gastrointestinal homeostasis. Regulation of hypoxia-mediated genes depends on the nuclear transcription factor, hypoxia inducible factor (HIF). HIF signaling is critical in the adaptive response to low oxygen levels by activating genes involved in metabolism, angiogenesis, cell survival and iron metabolism. Using the latest in mouse transgenic technology Dr. Shah has developed novel animal models to accurately study the role of oxygen sensitive transcription factors in the liver and intestine. The Shah laboratory has shown that hypoxic signaling is a critical regulator of systemic glucose homeostasis. In mouse models of obesity and diabetes, he has demonstrated that HIF2alpha signaling is activated rapidly and is important modulate intestinal incretin signaling and liver glucagon response. Building on this recent data, the Shah laboratory will identify mechanisms by which HIF2alpha signaling is increased via feeding cues and how HIF2alpha regulates glucose homeostasis.

Xin (Tony) Tong, M.D., Ph.D. is an Research Associate Professor in the Department of Molecular & Integrative Physiology. His research focuses on posttranslational modifications of transcription factors in glucose and lipid metabolism. Specifically, Dr. Tong’s team has been using a combination of genetic, molecular and biochemical approaches to elucidate the molecular mechanisms underlying SUMOylation of the transcription factor E4BP4 in the liver as well as its role during liver steatosis and liver fibrosis in a variety of diet-induced fatty liver disease mouse models.