Clee

Susanne Clee, Assistant Professor

Canada Research Chair in the Genetics of Obesity and Diabetes

Michael Smith Foundation for Health Research Scholar
Member, Diabetes Research Group, Life Sciences Institute

Postdoc: University of Wisconsin-Madison (2001-2007)
PhD: Genetics Graduate Program, University of British Columbia (1995-2001)
BSc (Hon): Biochemistry, Simon Fraser University (1994)

Office:  604-827-4271
E-mail:  susanne.clee@ubc.ca

 

R e s e a r c h   I n t e r e s t s

Obesity and diabetes are world-wide epidemics. The prevalence both of obesity and of type 2 diabetes has increased tremendously in the last decades. Currently over half the Canadian population, and greater than 1 billion individuals world-wide, are overweight or obese. Obesity is a major risk factor for many diseases including heart disease, type 2 diabetes, high blood pressure, cancer, sleep apnea, and infertility. Type 2 diabetes is an independent risk factor for heart disease, and a major contributor to kidney disease, blindness and limb amputations. Although we have made many advances in understanding the pathways underlying the regulation of food intake, insulin resistance, and insulin secretion, the specific defects that cause obesity and type 2 diabetes in the population are largely unknown. Genetic factors play a large role in determining which individuals will develop obesity and/or diabetes in the context of lifestyles with diets high in fat and calories and reduced exercise; however, the identities of most of these factors are unknown. In the Laboratory of the Genetics of Obesity and Diabetes we use genetics as a tool to gain insight into novel pathways promoting the development of obesity and type 2 diabetes.

The goal of my laboratory is to discover novel genetic factors contributing to the development of obesity and type 2 diabetes. Our research is focussed on identifying these genes and studying their function. We want to understand how the genes we identify contribute to disease risk. Our studies utilize genetic, molecular, cellular, and physiological approaches to gain a better understanding of the specific biological pathways that lead to the development of obesity and type 2 diabetes. This knowledge will suggest new ways that therapies can be designed to treat or prevent these diseases. These studies may also enable us to better diagnose individuals at higher risk of developing these diseases, either genetically or through the ascertainment of new biomarkers of disease. This would allow us to treat these individuals sooner and with the therapies most appropriate to their disease, which may also delay or even prevent the development of many of the debilitating complications associated with obesity and diabetes.

One current project in the lab will lead to the identification of a novel obesity-promoting gene. This gene was mapped in a cross between the BTBR and C57BL/6 inbred mouse strains. The underlying gene causes an approximately 10% increase in body weight in BTBR mice. Studies are currently underway to positionally clone this gene and understand the physiological mechanisms by which it affects body weight.

Another project in the lab involves the characterization of novel mouse strains for their risk of developing obesity and type 2 diabetes. These mouse strains will be used in future studies to identify additional genetic factors affecting obesity and diabetes risk, and will be important models for physiological studies to understand the cellular and molecular basis of these diseases.

S e l e c t e d   P u b l i c a t i o n s
  1. Ho MM, Johnson JD, Clee SM*. (2015) PWD/PhJ mice have a genetically determined increase in nutrient-stimulated insulin secretion. Mammalian Genome 26:131-141. [IF 2.9]. local collaboration
  2. Ho MM, Karunakaran S, Hu X, Johnson JD, Clee SM.* (2014) Altered pancreatic growth and insulin secretion in WSB/EiJ mice. PLoS One 9 2: e88352. [IF 3.5].local collaboration
  3. Liu S, Labouebe G, Karunakaran S, Clee SM, Borgland SL. (2013) Effect of insulin on excitatory synaptic transmission onto dopamine neurons of the Ventral Tegmental Area in a mouse model of hyperinsulinemia. Nutrition and Diabetes 3:e97. [IF 1.5].national collaboration
  4. Ho M, Yoganathan P, Chu KY, Karunakaran S, Johnson JD, Clee SM*. (2013) Diabetes genes identified by genome-wide association studies are regulated in mice by nutritional factors in metabolically relevant tissues and glucose concentrations in islets. BMC Genetics 14:10. [IF 2.4]. local collaboration
  5. Labouèbe G, Liu S, Dias C, Zou H., Wong JCY, Karunakaran S, Clee SM, Phillips A, Boutrel B, Borgland (2013) Insulin mediates long-term depression of VTA dopamine neurons via an endocannabinoid-mediated mechanism. Nature Neuroscience 16:300-8. [IF 15.3]. local collaboration
  6. Karunakaran S, Manji A, Yan CS, Wu ZJ, Clee SM*. (2013) The Moo1 obesity quantitative trait locus in BTBR T+ Itpr3tf/J mice increases food intake. Physiological Genomics 45:191-9. [IF 2.8].
  7. Yoganathan P, Karunakaran S, Ho MM, Clee SM*. (2012) Nutritional regulation of genome-wide association obesity genes in a tissue-dependent manner. Nutrition and Metabolism 9:65-75. [IF 2].
  8. Lee K, Karunakaran S, Ho MM, Clee SM* (2011) PWD/PhJ and WSB/EiJ mice are resistant to diet induced obesity but have abnormal insulin secretion. Endocrinology 152:3005-17. [IF 4.7].
  9. Bhatnagar S, Oler AT, Rabaglia ME, Stapleton DS, Schueler KL, Truchan NA, Worzella SA, Stoehr JP, Clee SM, Yandell BS, Keller MP, Thurmond DC, Attie AD. (2011) Positional Cloning of a Type 2 Diabetes Quantitative Trait Locus; Tomosyn-2, a Negative Regulator of Insulin Secretion. PLOS Genetics 7:e1002323. [IF 8.2].
Further publications can be found here.
J o i n   t h e   L a b
Positions are currently available. Interested individuals should email Dr. Clee directly and include a CV and description of relevant experience and interests