Dave Bridges, PhD is an Assistant Professor in the Department of Nutritional Sciences of the School of Public Health. His expertise is in understanding the genetic and regulatory mechanisms that result in response to macronutrient intake. His team’s primary research focus lies in understanding the molecular mechanisms that are deregulated in obesity, cardiovascular disease, and diabetes using a combination of mouse models and clinical data. The overall goals of his studies are to define the events involved in sensing and respond to nutrients to control the storage and transport of lipids and carbohydrates in the liver, adipose, and muscle. His team functions in a unique environment at the University of Michigan with ongoing collaborators in population genetics, dietary interventions, nutritional epidemiology, and basic research. They aim to integrate mechanistic research with rodent models of nutritional interventions with clinical- and population-based research to improve dietary management of chronic disease. Dr. Bridges has extensive experience mentoring undergraduate students both during the school year, and as part of summer training experiences such as that proposed in the M-SURE program. His laboratory typically has 2-4 trainees working at any given time including students from high school, in undergraduate programs or as medical students.
Eric Buras, MD, PhD is an Assistant Professor in the Division of Metabolism, Endocrinology & Diabetes with clinical and basic research interest in obesity. In the clinic, his practice is devoted to diagnosing and managing obesity complications, such as type 2 diabetes and hypoventilation. In the lab, he analyzes effects of over-nutrition on skeletal muscle structure and function, with special emphasis on the diaphragm. They have developed a workflow to evaluate obesity-related changes in diaphragm motion (non-invasive ultrasound) and contraction (ex vivo isometric force testing of muscle strips and single myofibers). Coupled with biochemical, histological, and cell-based (sc-RNA-seq, primary culture) analyses, this strategy generates a 3-dimensional picture of how this most critical skeletal muscle reacts to nutritional challenge. Dr. Buras is currently working to define the cellular and molecular players underlying effects of obesity and diabetes on skeletal muscle integrity—a program with future application to patient quality of life.
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.
Rodica Pop-Busui, MD, PhD is the Larry Soderquist Professor in Diabetes and the Vice Chair for Clinical and Health Outcomes Research in the Department of Internal Medicine at the University of Michigan. Her research lab, known as the Program for Diabetes Care and Complications Research, is dedicated to clinical research targeting new therapies and new technologies to fight against diabetes and its complications and advocating for implementing the optimal care for all patients with diabetes. She has participated as PI/co-PI in many landmark diabetes trials funded by NHLBI, NIDDK, or Pharma such as Action to Control Cardiovascular Risk in Diabetes (ACCORD). Many of these studies involve novel therapies, new technologies, and explore complications from cardiac neuropathy to optic complications to wound healing strategies. She is also working on projects to identify risk factors for diabetic patients who develop complications from COVID-19 disease. Dr. Pop-Busui has dedicated administrative space for herself and her team as well as shared clinical research space in many locations across the University system. Her team meets weekly for a 2-hour lab meeting, and the undergraduate trainees in this program will have access to herself as the PI, the Co-I’s in the lab, as well as her clinical research staff throughout the duration of the program. The trainee(s) will be immersed in clinical research projects within her lab.
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.
Eva Feldman, MD, PhD. is a Professor of Neurology. Dr. Feldman's laboratory focuses on the role of growth factors in neuronal growth and neuroprotection. The lab is specifically interested in the neurotrophic properties of the insulin-like growth factors I and II (IGF-I, IGF-II). They use molecular biology, gene therapy and protein biochemistry in their research. The lab primarily studies Amyotrophic Lateral Sclerosis (ALS) and Diabetic Neuropathy.
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.
Diane Fingar, PhD is an Associate Professor of Cell & Developmental Biology. She studies the regulation and function of mTOR signaling networks in mammalian cells and genetically modified mice. The kinase mTOR (mechanistic target of rapamycin) forms the catalytic core of mTOR complex 1 (mTORC1) and mTORC2, which sense and integrate diverse environmental cues to control cell and animal physiology appropriately. Aberrant mTOR complex (mTORC) signaling contributes to myriad pathologic states including metabolic disorders such as type II diabetes, immunological and cardiovascular disorders, and cancer. Dr. Fingar's lab additionally employs genetically modified mice to investigate mTOR crosstalk in control of physiology. Using CRISPR/Cas9, we have generated Mtor knockin mice resistant to AMPK- and TBK1-mediated phosphorylation. Ongoing research efforts focused on cultured cells and mouse models suggest that AMPK and TBK1 signal through mTOR complexes to regulate amino acid sensing and glucose and lipid homeostasis, particularly during diet-induced obesity.
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.
Dr. Giles is an Assistant Professor in the School of Kinesiology. Her lab primarily uses preclinical models (rodents & cell culture) to understand the link between obesity and breast cancer. Current projects are focused on understanding how weight gain during menopause and associated adipose inflammation contribute to breast cancer risk and progression, and using exercise, diet, and pharmacological interventions to decrease these obesity-associated comorbidities after menopause. Dr. Giles has mentored numerous undergraduate and graduate students in the lab, and welcomes students with an interest in obesity, metabolism, and cancer.
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.
Gary D. Hammer, M.D., Ph.D. is a Professor in the Departments of Internal Medicine (Metabolism, Endocrinology & Diabetes), Cell & Developmental Biology, and Molecular & Integrative Physiology. He is a past-president of the Endocrine Society. Research projects in his laboratory are aimed at elucidating the mechanisms by which growth factor signaling and transcriptional programs initiate adrenal- specific growth and differentiation with an emphasis on dysregulated adrenocortical stem cells in development and cancer. Collaborative work with colleagues has led to the development of international cooperative groups, most recently the A5 (American Australian Asian Adrenal Alliance) that leverages collaboration to secure projects from Pharma and funding agencies to advance research and clinical care across the spectrum of adrenal diseases. He is a co- founder of two companies - MILLENDO and most recently VASARAGEN that focuses on rare endocrine diseases and the development of new biological-based therapies that target molecular defects in disease while sparing normal tissue.
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.
Jun Hee Lee, PhD is an Associate Professor of Molecular & Integrative Physiology. His lab studies the relationship between stress, aging and metabolism. Previously, they showed the roles of Sestrins and autophagy in regulating stress responses and aging, which led to many important findings in the aging and metabolism fields. More recently, they expanded our stress response program into a new area of single cell, subcellular and spatial transcriptomics. Using a single cell RNA-seq (scRNA-seq) technique, we made several interesting findings indicating that a high level of heterogeneity exists in colon cancer responses to DNA damage and hepatocyte responses to obesity and fatty liver. They recently developed several new techniques to examine subcellular and spatial transcriptome including RG-RNA-seq, which can systematically characterize stress granule transcriptome in stressed cells, and Seq-Scope, which enables microscopic examination of spatial transcriptome for single cell and subcellular analysis.
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.
Ormond A. MacDougald, PhD is the John A. Faulkner Collegiate Professor of Physiology within the Molecular & Integrative Physiology department. To combat the rising incidence of obesity and associated metabolic diseases, the goal of his lab is to investigate how adipocytes throughout the body develop, function, and interact with other cell types near and afar.
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.
Liangyou Rui, Ph.D. is a Professor in the Molecular & Integrative Physiology Department. His laboratory studies the physiological and molecular mechanisms of obesity, fatty liver, and type 2 diabetes, using genetic, physiological, molecular, and biochemical approaches. Obesity is the primary risk factor for fatty liver disease and type 2 diabetes, and type 2 diabetes is caused by defects in both insulin production and insulin action (e.g. insulin resistance in the liver, muscle, fat and brain). Ongoing areas of study in the Rui laboratory include: 1) examining signal transduction pathways in hypothalamic neurons that regulate energy homeostasis, body weight and metabolism, 2) investigating molecular defects in hypothalamic neural circuits that cause leptin resistance, energy imbalance and obesity, and 3) studying glucose and lipid metabolism under both normal and obese conditions and focusing on the hepatic gluconeogenic and lipogenic programs as well as on the molecular mechanisms of insulin resistance in liver, adipose tissue and muscle.
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.
Randy Seeley, PhD is the Henry K. Ransom Endowed Professor of Surgery at the University of Michigan School of Medicine. He also serves as the director of the NIH-funded Michigan Nutrition Obesity Research Center (MNORC). His scientific work has focused on the actions of various peripheral hormones in the CNS that serve to regulate food intake, body weight and the levels of circulating fuels. His work has also focused on new treatment strategies for obesity and diabetes. He has published over 365 peer-reviewed articles. Collectively, this work has been cited more than 36,000 times and Dr. Seeley has a Scopus h-index of 98. Dr. Seeley has received numerous awards including the 2009 Outstanding Scientific Achievement Award from the American Diabetes Association. This award is presented to an individual medical researcher under age 45 who has made an outstanding contribution to diabetes research that demonstrates both originality and independence of thought.
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.
Kanakadurga Singer, M.D. is an Associate Professor of Pediatrics in the Endocrinology Division. Research in the Singer Lab is focused on understanding the influence of diet-induced obesity on hematopoiesis and the generation of activated macrophages that lead to metabolic disease. In obese adults and animal models, a chronic inflammatory state is closely linked to metabolic and non-metabolic diseases. She discovered that adipose tissue inflammation is driven by accumulation of monocyte-derived tissue macrophages rather than local macrophage expansion. Tracking these circulating monocytes to their origin led to her investigations of diet induced changes in hematopoietic stem cells and macrophage progenitor cells. Her laboratory has since identified that male mice, but not females, have an exaggerated myeloid inflammatory response in obesity which results in the accumulation and activation of adipose tissue macrophages. The striking differences between male and female diet-induced obesity has led to the current line of investigation in Dr Singer's research laboratory understanding how myelopoiesis is altered in those who are at risk for metabolic disease.
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.
Lei Yin, M.D., Ph.D. is an Assistant Professor of Molecular & Integrative Physiology. Dr. Yin’s lab investigates the functional link between insulin signaling and molecular clock in liver and its potential role in insulin resistance. Our initial results suggest that insulin signaling is tightly associated with circadian clock in liver cells, suggesting a functional crosstalk between these two pathways. We want to explore this finding using both cell culture and animal model. We have generated adenovirus for expressing or knocking down the core clock proteins and those reagents will be used to manipulate liver specific clock using tail-vein injection approach and then study insulin signaling and insulin function. The experimental approaches include RNA extractin, QPCR, protein isolation, immunoblotting as well as immunoprecipitation.