Insulin resistance, inflammation and the metabolic syndrome

Description of projects available to graduate students:
The focus of my group is to understand the biochemical and molecular mechanisms that link obesity, insulin resistance, dyslipidemia and inflammation in the metabolic syndrome (MS). MS comprises a clustering of risk factors (obesity, insulin resistance, dyslipidemia, inflammation, hypertension and altered thrombotic status) that dramatically increase the risk of developing diabetes and coronary vascular disease (CVD). As such MS is a serious public health problem that consumes excessive health care resources. Understanding the causes of MS and identifying biochemical drug targets for the treatment of MS is therefore a high priority. We are focusing our current research efforts on determining the mechanisms that link steatosis (excessive lipid storage in tissues) and insulin resistance and the role of increased activity of the innate immune system/inflammatory pathways in the pathogenesis of insulin resistance in obesity.

Techniques graduate student will learn:
Technologies:
(i) Molecular biological e.g quantitative gene expression analysis, recombinant adenoviruses for use in cell culture and whole animal,
(ii) Signaling pathway activity analysis e.g. insulin and leptin signaling through the IRS, phosphatidylinositol-3-kinase pathway in liver, immunoblotting,
(iii) Metabolic pathway activity e.g. analysis of carbohydrate and fat metabolism under conditions of obesity and altered inflammatory status in vivo

Model systems:
(i) Primary and immortal cell cultures derived from skeletal muscle, liver and adipose tissue.
(ii) Mice with conditional and whole body knockout of genes of interest
(iii) Obese and lean inbred Wistar rats