Prostaglandins (PGs) are a class of biologically active lipids involved in an array of physiological functions, including inflammation and insulin secretion. Two PGE2 receptors, EP3 and EP4, act in opposition to each other by signaling through different G proteins, resulting in activation (EP4) or inhibition (EP3) of adenylyl cyclase production. Loss of EP3 function has been shown to increase beta cell proliferation and mass as well as improve cardiac function, and activation of EP4 has similar effects on cardiac function, suggesting that modulation of these receptors may be beneficial for treating diabetes and cardiovascular disease. I am using mouse models of Type 2 diabetes to determine the effects of EP3 inhibition and/or EP4 activation on beta cell proliferation and survival and on cardiac function, as well as using rodent and human tissues to elucidate the downstream signaling pathways involved.