Common human diseases such as hypertension, diabetes and obesity can lead to serious complications such as heart attacks, congestive heart failure, kidney failure and early death. Both environmental and genetic factors contribute to these complex (multifactorial) diseases. Identifying their genetic component(s) will lead to better understanding of their dysfunctional mechanisms and improve our ability to prevent or more effectively treat their complications.
My laboratory uses physiological and comparative genomic approaches to identify genes and mechanisms leading to complex disease - hypertension, diabetes and obesity in particular - using both rat models and human populations. We use genetic linkage strategies to genetically map genes, and genetically unique rat strains to positionally clone and/or test candidate genes within a specific region of the genome. We then compare the genomes between the species, via comparative genomics, to translate the data from the rat to human and back again. Because the rat and human genes are 90% identical, it is likely the same genes or pathways will also play a role in many diseases.