Amanda Hall

Background:

Amanda is a general surgery resident at the University of Saskatchewan and is currently in the fourth year of her PhD through the Clinician Investigator Program. Her graduate work focuses on parenteral nutrition associated liver disease. In the course of her PhD program she has published a chapter on parenteral nutrition associated disease in infants in the text book Parenteral Nutrition: Policies and Procedures, Safe Practices and Potential Complications, (Nova Science Publishers Inc. 2014). She has also conducted a study separate from her main thesis investigating the aluminum levels in current neonatal parenteral nutrition (manuscript under review). Amanda has presented her research at the 2014 CAGS resident retreat and she looks forward to presenting at the 2016 American Society of Parenteral and Enteral Nutrition conference in January. After residency, she hopes to pursue a fellowship in pediatric surgery and continue nutrition-based research.

Research Summary:

Parenteral nutrition associated liver disease: the effects of aluminum contamination and lipid composition on bile acid transporter proteins.

Long term parenteral nutrition (PN) places newborn infants at risk of parenteral nutrition associated liver disease (PNALD), but the pathophysiology of this condition is still unknown. We theorize that both pro-inflammatory lipids and aluminum contamination contribute to PNALD. We hypothesize that by decreasing aluminum contamination and reversing pro-inflammatory lipid profiles, we can obtain the best preservation of bile acid transporters, thus preventing PNALD.

In partnership with Memorial University, we have conducted two randomized control trials using a newborn Yucatan miniature pig parenteral nutrition model. We have selected four bile acid transporters, and two supporting proteins as targets for this study. These targets will be examined by real time polymerase chain reaction (qPCR) to evaluate mRNA expression, immunofluorescence confocal microscopy to evaluate the localization of the bile acid transporters and Western blot to determine final protein presence. To date, we haveqPCR evidence that indicates the apical transporters (Mrp2 and Bsep) are both damaged by aluminum. The qPCR fold differences were 1.8 (SD 0.8) and 4.3 (SD 2.7) respectively, in favour of the low aluminum vs the high aluminum group. (Greater than 1.5 is significant). Further analysis is ongoing.

This work was made possible through grants from the Children’s Hospital Foundation of Saskatchewan, NSERC, and the University of Saskatchewan Department of Surgery.