Jane Shearer

The central focus of the Shearer laboratory is metabolic physiology. Our mission statement is to ‘Employ knowledge of metabolism to predict, prevent and treat chronic metabolic disease states’. Specific disease states of interest include obesity, cardiovascular disease and type 2 diabetes. Our genome to systems approach is unique provides the opportunity to examine both whole body and tissue specific biochemical and metabolic regulation. Specific laboratory projects are as follows:

Mitochondrial Physiology. Cardiovascular disease is the primary cause of morbidity and mortality in the industrialized world. The disease often cumulates in a myocardial infarction (MI) representing tissue death resulting from prolonged or extensive ischemia. Post-MI, heart failure is a significant concern with metabolic perturbations leading to progressive cardiac remodeling. A promising therapy for these conditions includes cell-based regenerative medicine that may one day lead to treatments to recover injured myocardium. Results generated in our laboratory and others show stem cells to alter metabolism, and this to be a key mechanism by which stem cells preserve injured tissue and promote healing.

Metabolic Influence of Post-translational Modifications. O-linked ?-N-acetylglucosamine (O-GlcNAc) modification is an intracellular tool capable of integrating energy supply with demand. The accumulation of excess energy associated with obesity and insulin resistance is mediated, in part, by the hexosamine biosynthetic pathway (HBP) that results in the O-GlcNAcylation of a myriad of proteins, thereby affecting their respective function, stability, and localization. Insulin resistance is related to the excessive O-GlcNAcylation of key metabolic proteins causing a chronic blunting of insulin signaling pathways and precipitating the accompanying pathologies, such as heart and kidney disease. Lifestyle modifications such as diet and exercise also modify the pathway.

Adenosine Receptor Antagonism. The adverse effects of acute caffeine consumption on glucose homeostasis are well-documented. Caffeine and related methylxanthines inhibit insulin-stimulated glucose uptake in the heart, isolated adipocytes and skeletal muscle preparations.  In humans, reductions (-30%) in whole body glucose disposal have been shown during both oral glucose tolerance tests and euglycemic-hyperinsulinemic clamps. Work in this area examines the metabolic impacts of caffeine-containing energy drinks on insulin resistance in lean and obese adolescents.

Research Areas: 

Molecular Biology and Disease

Lab Personnel

Melinda Wang, Lab Manager
Ning Cheng, Research Associate
Dr. Chunlong Mu, Postdoctoral Fellow
Dr. Oluyemi Falegan, Postdoctoral Fellow 
Dr. Wendie Marks, Postdoctoral Fellow
Shrusti Shah, PhD Student
Robyn Madden, PhD Student
Mishari Sjakhair, Undergraduate Thesis Student
Ali Abushaibah, Undergraduate Thesis Student
Abdul Abushaibah, Undergraduate Thesis Student
Christian Cao, Volunteer
Janelle Wai, Volunteer