Researcher investigating how hormonal changes impact risk of diabetes

Type 2 diabetes is one of the most common diseases affecting Canadians and a major contributor to premature death and disability. According to Diabetes Canada, up to 14 per cent of Canadians have diabetes, a condition that can reduce life expectancy by up to 15 years. 

Fat tissue keeps lipids from circulating in the body, helping prevent conditions like obesity, diabetes, insulin sensitivity and high cholesterol. Obesity is the biggest risk factor for Type 2 diabetes, making proper functioning of fat tissue critical in maintaining health. 

There are also sex differences when it comes to the risk of developing diabetes. Prior to menopause, women are less likely to develop type 2 diabetes than their male counterparts. That protection diminishes after menopause, but researchers aren’t sure why. 

Dr. Jennifer Thompson, PhD, an assistant professor in the Department of Biochemistry and Molecular Biology at the Cumming School of Medicine, suspects estrogen—acting at the cellular level—plays a key role.

She recently received a Diabetes Canada grant and bridge funding from the Canadian Institutes of Health Research to investigate her hypothesis that estrogen is involved in how fat tissue adapts to an environment that promotes weight gain. This mechanism may explain female-specific protection against diabetes and loss of that protection after menopause. 

“This is an exciting project that has the potential to fill a major gap in knowledge that remains with respect to female-specific factors in the development of diabetes,” says Thompson. 

Males tend to have unhealthy obesity, meaning they often develop other conditions, like high cholesterol, insulin insensitivity and high blood pressure. Males tend to develop these comorbidities at a younger age and lower body mass index than females. After menopause, females lose their advantage. 

The Thompson lab has been studying fat tissue, particularly the stem cells behind the formation of fat tissue (adipose progenitor cells), and their role in supporting healthy growth of fat tissue in an environment that promotes excessive weight gain.

Most of the current knowledge about the response of adipose progenitor cells in obesity has been learned through studies looking at male mice. Historically, female animals have been excluded from about 80 per cent of pre-clinical studies. 

“We are now looking at specific sex differences in adipose progenitor cells with the aim of understanding the role of estrogen,” says Thompson. 

Jennifer Thompson is an assistant professor in the Department of Biochemistry and Molecular Biology at the Cumming School of Medicine. She is a member of the Libin Cardiovascular Institute and the Alberta Children’s Hospital Research Institute.