Welcome to Czech Lab at UMass Chan Medical School

We apply new methods of gene silencing, editing, and deletion to better understand insulin signaling and energy expenditure pathways.

We share a common passion to translate our basic discoveries into therapeutic strategies for type 2 diabetes and obesity.

We collaborate with other scientists and companies to drive progress.

We welcome new lab members from diverse scientific backgrounds to join us!

Major human diseases such as type 2 diabetes and atherosclerosis are promoted by dysfunctions in adipose tissue and in the interactions between adipocytes, endothelial cells, nerve fibers and immune cells. Adipose tissue remodeling in obesity can also secondarily disrupt liver and skeletal muscle metabolism, causing systemic insulin resistance and glucose intolerance. Likewise, excess liver fat and muscle dysfunctions in obesity disrupt overall metabolic balance and communication. Our laboratory group is attacking key questions related to these cellular and molecular interactions among metabolic tissues, macrophages, neuronal signals and the vasculature that define both normal and metabolic disease states.

Central Interest  

Genes and their protein products that control metabolic health and are potential therapeutic targets for obesity and type 2 diabetes.

Central Questions

• Can we identify molecular mechanisms that disrupt insulin signaling in obesity and type 2 diabetes to develop therapeutic strategies for these diseases?
• Can we genetically modify adipocytes ex vivo with CRISPR technology to create cellular therapeutics for type 2 diabetes and its complications?
• Can we identify and modulate molecular mechanisms that switch adipocytes from storing triglyceride to cells that oxidize fat, expend energy, and secrete beneficial factors?
• Can we target genes that promote fatty liver and inflammation in obesity and diabetes with therapeutic siRNA to alleviate nonalcoholic steatohepatitis (NASH)?