McMaster University

Medical Sciences
Graduate Program

Scope of Search

Jonathan D. Schertzer

Jonathan D. Schertzer

Assistant Professor

Research Interests

The inability to respond to insulin is the major cause of type 2 diabetes. This insulin resistance precedes overt diabetes thereby providing therapeutic window to prevent the disease. Obesity is the main cause of insulin resistance and inflammation has emerged as a key link between obesity and insulin resistance. How does obesity cause inflammation and how does inflammation cause insulin resistance leading to diabetes? My laboratory is interested in understanding these problems in immunometabolism and how dietary and bacterial factors connect immunology and metabolism.

My laboratory attempts to understand how the food and drugs we ingest and the bacteria that colonize us can cause (or prevent) metabolic diseases. This work is particularly interested in how bacterial cell wall components or metabolic disease drugs (statins) alter metabolism via nucleotide oligomerization domain (Nod) or NOD-like (NLR) proteins. This research is complimentary to ongoing collaborative research on energy sensors and fat/glucose metabolism during obesity.

My laboratory is also very interested in the role of inflammation in muscle diseases (i.e. myopathies). Given that statin drugs are the first line treatment for obesity/diabetes related cardiovascular disease, we are particularly interested in immunity and statin-induced myopathy.


Health Sciences Centre
Room 4H30D

telephone: 905 525-9140 ext. 22254

Program Area

Physiology & Pharmacology

Research Focus


Selected Publications

  • Henriksbo BD et al., Fluvastatin causes NLRP3 inflammasome-mediated adipose insulin resistance. Diabetes. 2014
  • Chi W, Dao D, Lau TC et al., Bacterial peptidoglycan stimulates adipocyte lipolysis via NOD1. PLoS One. e97675, 2014.
  • Fullerton MD et al., Single phosphorylation sites in Acc1 and Acc2 regulate lipid homeostasis and the insulin-sensitizing effects of metformin. Nat Med. 19: 1649-54, 2013.
  • Gehrig SM, et al. HSP72 preserves muscle function and slows progression of severe muscular dystrophy. Nature, 484: 394-398, 2012
  • Hawley SA, et al. The ancient drug salicylate directly activates AMP-activated protein kinase. Science, Apr 19, 2012