Simon Fisher, MD, PhD, serves as the vice chair for research in the UK College of Medicine Department of Internal Medicine. Dr. Fisher is also the chief of the division of endocrinology and director of the Barnstable Brown Diabetes and Obesity Center. 

His research interests include the pathophysiology and treatment of diabetes, insulin action, tissue-specific crosstalk, complications of diabetes, neural glucose sensing, and hormonal counter-regulation. 

His laboratory provides an interactive and interdisciplinary environment that provides rigorous research training and scientific development of staff scientists, postdoctoral fellows, clinical fellows, MD/PhD students, PhD students, and undergraduate students who wish to pursue scientific careers in biomedical research.

Christopher Emfinger, PhD, is an assistant professor in internal medicine in the division of endocrinology and the Barnstable Brown Diabetes Center. The Emfinger lab focuses on identifying novel factors regulating metabolism and the ways in which these interact using both wet-lab and bioinformatic approaches.

Currently Dr. Emfinger’s work is focused on two main projects that apply machine learning approaches to predict islet-related functional traits (e.g. insulin secretion and plasma insulin). The first develops and validates novel ML models using omics data (e.g. sequencing, proteomics) to predict diabetes-relevant traits. The second focuses on identifying interactors for transketolase, an enzyme in the pentose phosphate pathway. Loss of this protein enhances islet function and its localization and pathway activity suggest a key non-metabolic role for TKT in islets. Identifying TKT’s interactors and ways to disrupt those interactions may provide novel therapeutic strategies for improving islet function in diabetes.

Future projects in the Emfinger lab will involve using sequencing data from key metabolic tissues (e.g. muscle, liver, adipose) to interrogate gene-gene dependencies between tissues and explore the role of inter-tissue communication in metabolic regulation.

Philip A. Kern, MD, is a professor of internal medicine in the division of endocrinology and co-director of the UK Center for Clinical and Translational Science. Dr. Kern’s research examines foundational mechanisms of the development of type 2 diabetes, including the roles of exercise and obesity to modulate insulin resistance, particularly in fat and muscle. Current research targets the role of beige and brown fat, circadian rhythms, inflammation, and changes in RNA structure. 

Dr. Kern’s research has been continuously funded by the National Institutes of Health (NIH) since 1986, he has coauthored over 200 research papers, and he is a mentor to many. In 2019, he was honored as a University Research Professor, the highest research award by the University of Kentucky. In 2023, he received the William R. Willard Dean’s Recognition Award for longstanding dedication to students and trainees.

Dr. Kern is an elected member of the American Society for Clinical Investigation (ASCI), an honorary society for clinician-scientists.

Preetha Shridas, PhD, is an associate professor of internal medicine in the division of endocrinology. The Shridas lab investigates the underlying mechanisms of chronic and acute inflammatory diseases, including cardiovascular disease, type 2 diabetes, and sepsis. High-density lipoprotein (HDL), traditionally regarded as the “good cholesterol,” is associated with a reduced risk of heart attack and stroke; however, during inflammation, HDL can become dysfunctional due to alterations in its protein composition, notably the incorporation of the acute-phase protein Serum Amyloid A (SAA).

The lab’s research focuses on elucidating how SAA modulates HDL functionality in different inflammatory contexts. The central hypothesis posits that while SAA contributes to HDL dysfunction in chronic inflammatory diseases, it paradoxically imparts a protective function to HDL in acute inflammatory states such as sepsis. This dual role positions SAA as a “double-edged sword,” providing protection in acute inflammation but exacerbating disease progression in chronic conditions such as atherosclerosis and abdominal aortic aneurysms. The lab aims to study the molecular mechanisms driving these divergent effects, thereby advancing our understanding of SAA’s complex role in inflammation.

Brian S. Finlin, PhD, is an assistant professor of internal medicine in the division of endocrinology. He is interested in how adipose tissue becomes dysfunctional in the context of obesity and in turn, impairs glucose and lipid homeostasis. Further, he is interested in possible therapeutic interventions. 

Dr. Finlin’s current research, in collaboration with Dr. Kern, involves the b3 adrenergic receptor agonist mirabegron, which has shown to improve glucose homeostasis, insulin sensitivity, and b cell function in humans. Dr. Finlin and Dr. Kern are currently investigating the molecular mechanisms by which this occurs, focusing on adipose tissue. They have identified several beneficial effects on adipose tissue and are in the process of identifying how these lead to the systemic effects described above.

Nate Helsley, PhD, is an assistant professor of internal medicine in the division of endocrinology. The Helsley Lablab investigates mechanisms by which fatty acid metabolism contributes to sexually dimorphic cardiometabolic disease and cancer phenotypes. The lab utilizes a combination of animal models, high throughput sequencing, and molecular approaches to probe these underlying mechanisms. 

Ila Mishra, PhD, is an assistant professor of internal medicine in the division of endocrinology. The Mishra lab investigates the cardiometabolic effects of asprosin, a newly discovered protein hormone. By combining advanced molecular biology, neuroscience, and mouse behavior and physiology studies, the Mishra lab research focuses on three core areas: uncovering novel neural roles of asprosin, developing breakthrough therapies to target it, and elucidating its cell signaling pathways. 

Recent work by Dr. Mishra has uncovered asprosin’s role in thirst regulation, identified its neural receptor for thirst and appetite stimulation, and developed monoclonal antibodies and receptor trap as therapeutics inhibiting asprosin function.

Qingzhang Zhu, PhD, is an assistant professor of internal medicine in the division of endocrinology and the Barnstable Brown Diabetes and Obesity Center. Dr. Zhu’s research focuses on the molecular and physiological characterization of novel proteins that mediate interactions between adipose tissue, the liver, and beta cells, with an emphasis on their therapeutic potential (please see publications 1-3 below).

Currently, he is investigating the progestin and adiponectin receptor family of proteins (PAQR1—11) and has identified specific members of this family with distinct roles in regulating ceramide homeostasis – an essential lipid species involved in diverse cellular functions.

Dr. Zhu anticipates that his future research will focus on uncovering the molecular mechanisms underlying ceramide overload, a hallmark of metabolic disorders, and in exploring the physiological roles of PAQR-mediated ceramide pathways in adipose tissue and inter-organ communication during obesity and related diseases.

Sathya Velmurugan, PhD, is an Assistant Professor (Research Title Series) in Dr. Simon Fisher’s lab in the Department of Internal Medicine division of endocrinology, diabetes and metabolism. 

Her research focuses on defining the mechanisms underlying hypoglycemia-induced cardiac arrhythmias in diabetes. Her work integrates in vivo and cellular models to investigate how recurrent moderate hypoglycemia and severe hypoglycemia alters cardiac electrophysiology, calcium handling, and mitochondrial stress signaling. By combining physiological, cellular and molecular approaches, her studies aim to identify adaptive and maladaptive stress pathways and biomarkers that predict arrhythmia susceptibility and cardiac injury, with the long-term goal of developing strategies to prevent hypoglycemia-associated cardiovascular complications.