Our Research Members

Dr. Hahn is a clinician-scientist at the CAMH whose research interests lie in translational work focused on the complex interplay between mental illness, antipsychotic treatments, and cardiometabolic risk, with a special interest in type 2 diabetes. Given the early accrual of metabolic risk leading to a 20% reduction in life expectancy for patients with schizophrenia and other severe mental illnesses, she has an interest in treatment and prevention strategies of so called “modifiable” cardiovascular risk factors. She is leading a number of clinical trials focus on targeted pharmacological interventions to reduce metabolic burden and improve other domains of health (i.e. psychopathology, cognition, quality of life) in this population. She is the director of the Mental Health and Metabolic Clinic at the CAMH, which specializes in metabolic monitoring, and interventions for metabolic risk factors in individuals with serious mental illness. She also oversees a basic science laboratory which conducts cutting edge research examining mechanisms (focusing on the central nervous system) of high rates of obesity and diabetes in those receiving psychotropic treatments. Dr. Hahn holds the Cardy Schizophrenia Research Chair at CAMH.

My research interests include the clinical and physiologic manifestations of insulin resistance and pancreatic beta cell function in the pediatric age group. I am also interested in treatment studies of childhood obesity. Recent studies include:

(i) risk for diabetes and metabolic syndrome and pathophysiologic mechanisms related to the development of hypothalamic obesity in children treated for craniopharyngioma;
(ii) early life risk factors for the development of obesity and diabetes in infants born to women with gestational diabetes;
(iii) incidence and clinical presentation of type 2 diabetes in Canadian children
(iv) evaluation of eating behaviours and traits in children and adolescents attending weight management programs in Canada
(v) bariatric surgery outcomes in adolescents

Dr. Hanley’s research interests include the metabolic and nutritional epidemiology of type 2 diabetes and related disorders including obesity, insulin resistance, and beta cell dysfunction, as well as the micro-and macro-vascular complications of type 2 diabetes. His research focuses on diabetes in Indigenous Canadian communities and other high-risk populations. Current projects include the Sandy Lake Health and Diabetes Project, the PROMISE study, as well as collaborations with the Insulin Resistance Atherosclerosis Study and the Gestational Diabetes and Acute Phase Biomarkers research groups.

I am a clinical epidemiologist/health services researcher in the field of osteoarthritis (OA) – I have conducted observational studies examining the relationship between OA and diabetes. Among other findings, we have shown that difficulty walking due to hip or knee OA is an independent risk factor for diabetes complications in people with OA and diabetes, and also a risk factor for incident diabetes.

Many physiologic processes are mediated by a group of switch-like heterotrimeric G proteins. G proteins are normally coupled to receptors on the cell surface to act as intracellular relays between environmental stimuli and the rest of the cell. Our work defines the biologic importance for precise kinetic regulation of G-protein-mediated signaling events.

Regulation of G-protein signaling pathways: The G-protein heterotrimer is composed of a GDP-bound G alpha subunit and a G beta gamma heterodimer. Upon G-protein activiation, the Galpha subunits are free to engage appropriate downstream effector pathways. Effector signaling is terminated following G alpha catalysed hydrolysis of GTP and reformation of the quiescent receptor-coupled heterotrimer. RGS proteins are a family of GTPase activating proteins (GAPs) for G alpha subunits. By increasing the intrinsic rate of GTP hydrolysis for G alpha subunits, RGS proteins impact GPCR-mediated signaling pathways by: i) promoting faster signal termination kinetics following removal of a physiologic GPCR agonist; and ii) decreasing GPCR agonist sensitivity (i.e. higher agonist concentrations are needed to achieve the same degree of signaling). Our work is aimed at defining the molecular mechanisms that regulate the function of RGS proteins in vivo . Using a combination of physiology, biochemistry, cell biology, pharmacology, and genetics we examine how subcellular localization, G-protein selectivity and interaction with other cellular signaling components regulates the function of RGS proteins in living organisms.

Regulation of G-protein signalling in Pancreatic Islet beta cells: Previous work has shown that one RGS protein family member, RGS4, is highly expressed in beta cells and its function can have profound physiologic effects on insulin secretion. Although the majority of the work in this field has been focussed on the role of RGS4 at the plasma membrane, our recent studies have identified a novel intracellular location for RGS4, the preautophagosome, where it can regulate the autophagic flux and metabolic homeostasis within beta cells. Notably, activated Galphai3 is a potent attenuator of autophagic activity. Accordingly, our work is aimed at understanding the role of RGS4 in the regulation of autophagic flux and enery homeostasis in pancreatic islet beta cells.

Diabetes-related injuries affect virtually all the major organs, leading to an epidemic of macrovascular and microvascular complications that lead to organ failure. My research program is focused on developing novel imaging modalities for the examination of diabetic-related injuries in various organs such as the kidney, liver, heart, and skin. I direct the Translational Ultrasound and Photoacoustic Imaging Laboratory (TUPIL) at St. Michael’s Hospital. I am particularly interested in quantitative ultrasound and photoacoustic imaging, two related modalities that have a lot of potential for simultaneous examinations of whole organ structure and function, across multiple biological length scales. Our techniques are capable of assessing vascular injuries, and their impact on organ fibrosis. These modalities have been deployed in preclinical studies in the kidney and liver, and are currently used in a clinical trial at St. Michael’s Hospital in assessing the degree of fibrovascular injury in kidney transplants, which are often impacted by diabetic nephropathies present in donors.