title: The route of lipid administration affects parenteral nutrition-induced hepatic steatosis in a mouse model.
abstract: BACKGROUND
  The etiology of parenteral nutrition (PN)-associated hepatic injury remains unresolved. Recent studies have suggested that the intravenous (IV) lipid emulsion administered with PN may contribute to PN-associated hepatic injury. We therefore examined whether the route of lipid administration would affect the development of PN-associated liver injury in a previously established animal model of PN-induced hepatic steatosis.
  
  
  METHODS
  Mice were fed ad libitum PN solution as their only nutritional source for 19 days with lipid supplementation by either the enteral or the IV route. Control mice received chow alone, and a final group received enteral PN solution without lipid supplementation.
  
  
  RESULTS
  All mice gained equivalent weight during the study. Mice receiving PN alone or PN with IV lipid developed severe histologic liver damage that was not seen in control mice or in mice receiving PN with enteral lipid. Liver fat content as measured by magnetic resonance spectroscopy was significantly lower in the control and enteral lipid groups when compared with mice receiving PN alone or with IV lipid. Mice receiving enteral lipid had significantly lower levels of serum aspartate aminotransferase and alanine aminotransferase compared with animals receiving PN alone.
  
  
  CONCLUSIONS
  These data provide preliminary evidence that lipid administered through the enteral route protects against PN-associated hepatic injury in an animal model.
authors.affiliation: Department of Surgery, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA.
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: Javid
authors.forename: Arin K
authors.initials: AK
authors.lastname: Greene
authors.forename: Jenna
authors.initials: J
authors.lastname: Garza
authors.forename: Kathleen
authors.initials: K
authors.lastname: Gura
authors.forename: Ian P J
authors.initials: IP
authors.lastname: Alwayn
authors.forename: Stephen
authors.initials: S
authors.lastname: Voss
authors.forename: Vania
authors.initials: V
authors.lastname: Nose
authors.forename: Ronit
authors.initials: R
authors.lastname: Satchi-Fainaro
authors.forename: Blanca
authors.initials: B
authors.lastname: Zausche
authors.forename: Robert V
authors.initials: RV
authors.lastname: Mulkern
authors.forename: Tom
authors.initials: T
authors.lastname: Jaksic
authors.forename: Bruce
authors.initials: B
authors.lastname: Bistrian
authors.forename: Judah
authors.initials: J
authors.lastname: Folkman
authors.forename: Mark
authors.initials: M
authors.lastname: Puder
mesh_terms: D000818:Animals; D004041:Dietary Fats / Q000009:adverse effects; D004195:Disease Models, Animal; D004750:Enteral Nutrition / Q000009:adverse effects*; D005234:Fatty Liver / Q000209:etiology*; D008055:Lipids / Q000008:administration & dosage / Q000009:adverse effects* / Q000493:pharmacokinetics; D008099:Liver / Q000473:pathology; D008279:Magnetic Resonance Imaging; D051379:Mice; D008810:Mice, Inbred C57BL; D010288:Parenteral Nutrition / Q000009:adverse effects*; D015430:Weight Gain
chemical_list: D004041:Dietary Fats; D008055:Lipids