When I finished my undergraduate degree, I was offered an exciting opportunity to spend 6 months at the Nestlé Research Centre in Switzerland. And I found out that Nestlé does far more than just make good chocolate! Nestlé introduced me to the field of nutrigenomics. This area of research examines how the foods we eat interact with our genes to affect our health. Working in this fascinating area allowed me to integrate various scientific disciplines into my research, ranging from nutritional biochemistry and molecular biology to genomics and bioinformatics. My initial 6 month position with Nestlé ended up becoming a 6 year stay, during which I completed my PhD in association with the University of Lausanne. After finishing my PhD, I moved to The Scripps Research Institute in San Diego, USA for a short post-doctoral position and then to the Institut National de la Santé et de la Recherche Médicale (INSERM) in Paris, France for a second post-doctoral position. During my post-doctoral research I explored diet-gene interactions in the context of obesity. This proved both timely and highly relevant given the high prevalence of obesity. Obesity is a complex disease that is highly influenced by an individual’s lifestyle habits (e.g., diet and exercise). Importantly, each of these habits influences our genes and, ultimately, our health. In 2009, I joined the Department of Human Health & Nutritional Sciences to establish a nutrigenomics research program to study how dietary fats regulate gene expression in metabolic tissues, and how this contributes to the development of obesity-related complications.
B.Sc. Queens University (Canada) Ph.D. University of Lausanne (Switzerland)
Obesity is a primary risk factor for type-2 diabetes and cardiovascular disease. Generally speaking, obesity occurs when energy intake outweighs energy expenditure. The prevalence of overweight and obesity in Canadian adults is greater than 60%. In other words, 3 out 5 adults in Canada have excess bodyweight that increases their risk for chronic disease. My nutrigenomics research program investigates the mechanisms that regulate lipid metabolism in the body, with a primary focus on diet-gene interactions in adipose (fat) tissue. Dysfunctional lipid metabolism is a key feature of obesity, and an underlying cause for many of the downstream consequences associated with obesity, such as inflammation and insulin resistance. My team is specifically interested in a family of enzymes known as desaturases, which are critical in fatty acid synthesis. We have recently discovered that inhibition of delta-6 desaturase (D6D) protects against lipid accumulation in adipose tissue and partially prevents high-fat diet-induced impairments in glucose tolerance. What remains unclear is how these outcomes occur, and this knowledge is imperative for the development of novel therapeutics or diet interventions that target desaturase activity. Ongoing research in my lab uses cell and rodent models to explore how reduced desaturase activity influences adipogenesis, lipogenesis, and lipolysis. Most notably, our research is immediately translatable and has important implications for humans. Indeed, humans with genetic variations in the D6D gene (~30% of the general population) show many of the same metabolic outcomes as our model systems in which desaturase activity is inhibited. For example, we have reported that variants in desaturase genes influence fatty acid profiles, fat oxidation, and adipose tissue inflammation. Our research in this area is unique and novel for a number of reasons. First, we are one of the few labs worldwide to have the desaturase knock-out mouse model. Second, my program interchanges between cell, rodent, and human models to advance our understanding of these key enzymes.
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