Our Research Members

The focus of Dr. Danska’s research is defining mechanisms of immune mediated diseases and application of this knowledge to improve their diagnosis, prevention and treatment.  Her lab works on the genetic and environmental causes of autoimmune disease, particularly Type 1 diabetes (T1D) in animal models and prospective human cohort studies. Her group found that manipulation of the intestinal microbial community (microbiome) strongly influences levels of sex hormone levels, host metabolites and can protect mice with high inherited risk from T1D.  She has led international projects that identified diabetes risk genes and determined how these variants control immune pathogenesis.  Her current work is focused on identification of environmental factors responsible for the rise in rates of autoimmune and inflammatory diseases, and how these factors are modified by the intestinal microbiome. She has a long-standing interest in sex as a determinant of autoimmune disease risk and pathogenesis.

I am interested in obesity and insulin resistance. More specifically I aim to assess the role of the central nervous system in mediating various metabolic processes in humans in responses to drugs and peptides. Another avenue of research I will explore is investigating the etiology of obesity, its metabolic complications and response to treatment. I aim to utilize a combination of integrative in vivo physiology, genetic and pharmacological approaches to answer these research questions with the ultimate aim of potentially developing novel therapies for metabolic disorders.

I pursue population-based health services research focusing on patients with diabetes who undergo lower limb amputation. I am interested in better characterizing the epidemiology, outcomes, health-resource use and costs of lower limb amputation in diabetic patients as well as limb preservation therapies. The purpose of this work is to inform population-level interventions to reduce diabetes-related foot complications.

My lab is interested in skeletal muscle biology and how phosphoinositides regulate the transport of vesicles within the muscle and how they govern exocytosis. This has direct relevance to diabetes, as these pathways are critical for regulating insulin dependent GLUT4 trafficking and, as such, muscle dependent regulation of insulin sensitivity. PIPs and their regulatory enzymes also influence secretion of myokines. Myokines are critical for muscle crosstalk with other organs, including the brain, liver, and adipose tissue. Muscle dependent organ cross talk is an emerging area of regulation of whole body metabolism, and can influence development of diabetes and modulate its sequelae. Lastly, we are very interested in therapy development. We hypothesize that modulation of the PIP pathway will provide a novel, muscle specific treatment strategy for diabetes. We are actively working on developing such a therapy, targeting specifically one of the PIP enzymes.

Research in the Drucker lab is focused on understanding the biology of gut hormones, with a major focus on GIP and the glucagon-like peptides. The lab studies how glucagon, GIP, GLP-1, and GLP-2 regulate energy homeostasis, metabolic control, and cardiovascular function via effects on the gastrointestinal tract, pancreas, cardiovascular system and central nervous system. Specific projects elucidate novel mechanisms of glucagon, GIP, GLP-1 and GLP-2 action through studies of their respective receptors in peripheral tissues. Research staff utilize a combination of techniques that involve studies of signal transduction, generation of transgenic or knockout mice, and studies of rodent models of peptide hormone action with a focus on diabetes, obesity, endocrine systems, and intestinal disease.