The primary basic research focus of our lab has been to elucidate the roles of placental and fetal hormones in the regulation of maternal metabolism and fetal growth. Prolactin receptor (PRLR) signaling has been implicated in the pathogenesis of obesity, polycystic ovary syndrome, ovarian failure, and cancers of the prostate and breast. The major goal of our research is on the preservation of beta cell function as a means for preventing and treating diabetes mellitus (1,2) .
Recently we have generated a mouse with a targeted deletion (“knockout”, KO) of the prolactin receptor (PRLR) in pancreatic beta cells. This new experimental model will be used to probe novel mechanisms in the control of beta cell mass, insulin production during pregnancy and postnatal life. Our findings will have implications for the pathogenesis, prevention, and treatment of neonatal glucose intolerance and gestational diabetes (GDM).
We also have a clinical research interest in the pathogenesis and treatment of obesity and hyperlipidemia and the prevention of type 2 diabetes. In previous studies we showed that the drug metformin reduces fat stores and blood glucose and insulin levels in obese adolescents and may reduce the risk of progression to diabetes in selected patients (3,4). We have also examined the unique metabolic characteristics of Prader Willi syndrome, a genetic obesity disorder (5). More recently, we have completed a detailed study of metabolism in malnourished children in Uganda and characterized the effects of concurrent HIV infection on nutritional recovery (6).