Dr. Gumus Balikcioglu did her medical training at Hacettepe University, School of Medicine, Ankara, Turkey. After medical school, Dr. Gumus Balikcioglu completed a residency and chief residency in pediatrics at Hacettepe University, Department of Pediatrics, Ankara, Turkey. She completed a fellowship in pediatric endocrinology at Louisiana State University, Health Sciences Center, New Orleans, LA. In order to meet licensing requirements, she completed a second pediatric residency at the University of North Carolina, School of Medicine, Chapel Hill, NC. In September 2013, Dr. Gumus Balikcioglu joined the faculty at Duke University, Department of Pediatrics, Division of Pediatric Endocrinology. She has had a longstanding interest in the pathogenesis and predictors of progression to Type 2 Diabetes in children.  She used targeted metabolic profiling of fasting and post-prandial plasma samples to identify metabolic signatures of insulin resistance in obese adolescents and children with Prader Willi syndrome. She is now exploring the use of non-targeted metabolic profiling of 24-hour samples of urine, which has the advantage over single point-in-time plasma samples of integrating differences in metabolic status over time for metabolic assessment of diabetes risk in children.

Using metabolomic analysis of plasma and urine, Dr. Gumus showed that insulin resistance in obese adolescents is positively associated with a metabolic “signature” comprising the branch chain amino acids (BCAA) and uric acid. Her more recent studies implicate a novel role for serotonin metabolism in the pathogenesis of childhood type 2 diabetes. She now proposes to elucidate possible cellular mechanisms by which BCAA and serotonin interact in the control of glucose stimulated insulin secretion in pancreatic beta cells. She postulates that elevations of BCAA limit the uptake of tryptophan into pancreatic beta cells; this in turn reduces beta cell serotonin production and insulin secretion, promoting glucose intolerance in high risk, insulin resistant subjects. To test this hypothesis, she proposes laboratory-based mechanistic studies of islet cell biology, which include the impact of overexpression, or suppression of the large neutral amino-acid transporter (LAT1) amino acid carrier on islet cell phenotypes under various nutritional conditions. If these mechanistic studies prove that reductions in tryptophan availability and serotonin production inhibit insulin secretion, then future studies targeting the tryptophan/serotonin pathway and LAT1 could provide new therapeutic approaches for diabetes prevention and treatment.

MHS Duke University School of Medicine

MD Hacettepe University (Turkey)

Publications List