Obesity and associated metabolic disease such as type 2 diabetes continue to be the leading cause of preventable death worldwide. Additional research into novel treatments beyond our current options are therefore warranted. One promising experimental approach to correct the metabolic dysfunction associated with obesity is to activate brown fat non-shivering thermogenesis. The Barrow lab leverages various proteomics, transcriptomics, and metabolomic platforms paired with custom AAV viral targeting, and genetic mouse models to uncover novel molecular targets that harbor therapeutic potential to combat obesity at the molecular level.

Mitochondrial disease encompasses a heterogeneous group of disorders that originates either from maternally-inherited genetic mutations in mitochondrial DNA or from somatic mutations in the nuclear genome. These mutations typically impair the mitochondrial electron transport chain (ETC) system responsible for the generation of ATP and if uncorrected will lead to death. There is currently no option of a cure or effective therapy. The Barrow lab uses high throughput screening platforms in physiologically-relevant systems such as primary muscle stem cells and genetic mouse models to identify small molecules that can overcome mitochondrial dysfunction. 

It is still unknown why certain individuals respond to dietary treatments and interventions while other groups do not. The Barrow lab investigates various nutrient-gene interactions in humans beginning at the human level with comprehensive dietary interventions and nutrition assessments, and then taking a deep molecular dive to unveil mechanisms to understand the human precision nutrition response.