Samer El-Kadi

• Ph.D., Animal Science, 2006, University of Maryland
• M.S., Poultry Science, 2000, American University of Beirut, Lebanon
• Diploma, Agriculture Engineer, 1998, American University of Beirut, Lebanon
• B.S., Agriculture, 1998, American University of Beirut, Lebanon

My research program is focused on understanding how early nutritional exposures shape metabolic development, with particular emphasis on neonatal and pediatric nutrition. Using the neonatal pig as a translationally relevant model for the human infant, my laboratory investigates how dietary composition, particularly lipids and amino acids, influences metabolism in the liver, skeletal muscle, and gastrointestinal tissues during critical windows of early development.

A central focus of our current work is the developmental origins of metabolic disease. We have demonstrated that medium-chain fatty acid feeding in neonatal pigs rapidly induces hepatic steatosis and can progress to steatohepatitis within days, establishing a novel pediatric model for studying early-onset liver disease. Beyond the liver, we have shown that early dietary lipid composition simultaneously reprograms metabolic pathways in skeletal muscle, underscoring the systemic consequences of infant nutritional exposures.

Low birthweight represents another major focus of our research. Neonates born with this condition exhibit significant defects in protein synthesis and are at heightened risk for impaired growth and lifelong metabolic disease. Our work has revealed that while aggressive nutritional intervention can enhance growth in low birthweight neonatal pigs, it paradoxically elevates hepatic fat deposition, a precursor to metabolic disease, highlighting the inadequacy of traditional nutritional approaches and the urgent need for targeted interventions that address the underlying metabolic vulnerabilities imposed by low birthweight.

A complementary area of our research examines how feeding practices and nutrient delivery influence protein metabolism and lean tissue accretion in neonates. Our work has demonstrated that intermittent bolus feeding stimulates greater protein synthesis than continuous feeding through enhanced activation of insulin and amino acid signaling, with direct implications for the nutritional management of hospitalized infants.

To address these questions, we employ a multifaceted approach combining multi-catheterized animal models, stable isotope tracer techniques, 13C-mass isotopomer distribution analysis (MIDA), and primary cell culture systems to resolve nutrient fluxes and metabolic pathway activity at the tissue level.