Project 467078

The prevalence of type 2 diabetes T2D continues to rise, with the International Diabetes Federation estimating 700 million affected individuals by the year 2045. Mirroring the rise of diabetes is the large increase in age-related muscle disease. Muscle plays a critical role in normalizing blood sugar levels. Thus, abnormal muscle function can exacerbate T2D. There are many factors that influence how muscles function. Specifically, studies have linked Janus Kinase 2 (JAK2), a protein that moderates responses to various signals in cells, to compromised muscle function. This link suggests that JAK2 protein may have a role in T2D. Consequently, our research will explore the role JAK2 plays in muscle function and diabetes. We will create a mouse model that lacks the JAK2 only in muscle, and use this model to further our understanding of the JAK2s role in muscle function and diabetes. Our tests will include determining whether mice that lack JAK2 develop diabetes or abnormal muscle function. We will also assess whether body weight or muscle weight is affected by JAK2 deletion in muscle. Currently, our preliminary data show that mice that lack JAK2 only in muscle weigh less and have smaller muscles than control mice that express JAK2. This suggests muscle JAK2 plays an important role in muscle health. Given the rising disease burden of T2D, our research can help identify new drug targets for the prevention and treatment of diabetes and muscle dysfunction.