Michael Freemark, MD

Faculty Member, Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center

Position

Atkins Professor Chief, Division of Pediatric Endocrinology and Diabetes Department of Pediatrics Duke University Medical Center

Contact

Lenox Baker Children's Hospital 3000

919 684 8350

michael.freemark@duke.edu

Summary

Michael Freemark is the Atkins Professor of Pediatrics and Chief of the Division of Pediatric Endocrinology and Diabetes. The lab's research scientist is Ramamani Arumugam, PhD. Drs. Freemark and Arumugam have a longstanding interest in the roles of placental and pituitary hormones in the regulation of maternal metabolism and fetal growth. Using novel transgenic and knockout models of lactogen action, they focus on the control of beta cell development and function during the perinatal period and pregnancy and the defense against type 2 diabetes. 

MD, Duke University, Durham, NC

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).

Staff

Ramamani Arumugam, PhD