Nadia Rachdaoui

Assistant Research Professor
Endocrine Research Facility
848-932-5576
rachdaoui@sebs.rutgers.edu

Curriculum Vitae (86k PDF)

Publications

Research

I have two primary research interests.

First, the worldwide obesity epidemic represents a major risk factor for the development of insulin resistance and diabetes. Obesity-associated insulin resistance plays a causative role in the development of hyperinsulinemia. Although the role of hyperinsulinemia in the development of peripheral insulin-resistance has been proposed and extensively studied, the role of hyperinsulinemia in pancreatic beta-cell dysfunction is understudied. My interest lies in determining the molecular and signal-transduction mechanisms involved in the hyperinsulinemia-induced defects in pancreatic beta-cell function and survival in the context of obesity-mediated diabetes. I study the role of the insulin/IGF-1 signaling pathways in maintaining pancreatic beta-cell function and survival. This has special meaning in the context of the Accelerator Hypothesis, which proposes that, in association with autoimmunity, insulin resistance accelerates the rate of pancreatic beta-cell apoptosis. This is particularly important as we are witnessing a sharp increase in childhood obesity with a parallel rise in the incidence of Juvenile Type 1 Diabetes. My studies take advantage of models where dietary interventions can be used to induce obesity across stages of development (e.g. young vs adult rodents), we then contrast the effects of hyperinsulinemia on pancreatic islet (beta-cell) health and function.

Second, alcohol consumption during pregnancy is a significant public health problem that can result in a continuum of adverse outcomes to the fetus known as fetal alcohol spectrum disorders (FASD). These disorders range from growth retardation to neurobehavioral alterations. Epigenetic alterations may mediate some of the deleterious effects of fetal alcohol exposure and therein contribute to the deficits that are observed in FASD. Our central hypothesis is that histone turnover might be an important parameter that can contribute to the alcohol-mediated epigenetic alterations which result in defective expression of developmentally important genes. In collaboration with Dr. Dipak Sarkar, we couple the use of a novel stable isotope tracer method with standard proteomic analyses (LC-MS/MS) to explore dynamic changes in histone kinetics in a rodent model of postnatal alcohol exposure (mimicking the third trimester of human pregnancy). In addition, we are investigating how defects in the DNA damage response can impact the epigenetic processes, particularly histone turnover and deposition in chromatin.

Experience

Education