Supplemental Parenteral Vitamin E Into Conventional Soybean Lipid Emulsion Does Not Prevent Parenteral Nutrition–Associated Liver Disease in Full‐Term Neonatal Piglets |
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Authors: | Mitsuru Muto MD PhD David Lim MD CM Amanda Soukvilay BScN Catherine Field PhD Pamela R Wizzard BSc Susan Goruk Ronald O Ball PhD Paul B Pencharz MD PhD Si Mi MSc Jonathan Curtis PhD Paul W Wales MD MSc Justine M Turner MD PhD |
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Institution: | 1. Department of Pediatrics, University of Alberta, Canada;2. Department of Surgery, University of Alberta, Canada;3. Department of Agricultural Food and Nutritional Science, University of Alberta, Canada;4. Department of Gastroenterology and Nutrition, Hospital for Sick Children, Toronto, Ontario, Canada;5. Group for Improvement of Intestinal Function and Treatment, Hospital for Sick Children, Toronto, Ontario, Canada;6. Division of General Surgery, Hospital for Sick Children, Toronto, Ontario, Canada |
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Abstract: | Background: Parenteral nutrition–associated liver disease (PNALD) continues to cause morbidity and mortality for neonates with intestinal failure. Lipid peroxidation is one potential etiological factor. This study was designed to test if supplementing vitamin E into conventional soy‐based lipid would reduce the risk of PNALD. Methods: Sixteen piglets, aged 2–5 days and weighing 1.8–2.5 kg, were randomized to parenteral nutrition (PN) with soy lipid (SO, n = 8) or the same lipid plus α‐tocopherol, the most bioactive form of vitamin E (SO+E, n = 8). After 17 days, bile flow, liver chemistry, gene expression associated with bile acid metabolism, and bile acid composition were assessed. C‐reactive protein (CRP) and oxidative stress markers, including plasma 8‐isoprostane, were measured. All results were compared with a sow‐reared control group (CON). Results: Comparing PN‐treated groups, SO vs SO+E mean bile flow (5.91 vs 5.54 µL/g liver; P = .83), serum bile acid concentration (39.2 vs 26.6 µmol/L; P = .12), and total bilirubin (35.2 vs 26.9 µmol/L; P = .56) were not different. Gene expression related to bile acid metabolism and bile composition was not different between PN groups. There was no difference in CRP (41.8 vs 36.8 µg/mL; P = .22) or in plasma 8‐isoprostane (27.9 vs 26.1 pg/mL; P = .77). Conclusions: In term neonatal piglets, supplemental vitamin E did not prevent cholestasis. Additional vitamin E was not associated with reduced inflammation or oxidative stress. The benefit of supplementing vitamin E into conventional lipid, vs adding fish oil, to prevent early onset of PNALD requires further clarification. |
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Keywords: | vitamin E α ‐tocopherol parenteral nutrition parenteral nutrition– associated liver disease lipid peroxidation cholestasis |
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