title: Lipid emulsion administered intravenously or orally attenuates triglyceride accumulation and expression of inflammatory markers in the liver of nonobese mice fed parenteral nutrition formula.
abstract: The accumulation of hepatic TG and development of hepatic steatosis (HS) is a serious complication of the use of parenteral nutrition (PN) formulas containing a high percentage of dextrose. But whether fat emulsions or other nutrients can ameliorate the induction of HS by high-carbohydrate diets is still uncertain. We hypothesized that administration of a lipid emulsion (LE; Intralipid) and/or the vitamin A metabolite retinal (RAL) will reduce hepatic TG accumulation and attenuate indicators of inflammation. C57BL/6 male mice were fed PN formula as their only source of hydration and nutrition for 4-5 wk. In Expt. 1, mice were fed PN only or PN plus treatment with RAL (1 μg/g orally), LE (200 μL i.v.), or both LE and RAL. In Expt. 2, LE was orally administered at 4 and 13.5% of energy to PN-fed mice. All PN mice developed HS compared with mice fed normal chow (NC) and HS was reduced by LE. The liver TG mass was lower in the PN+LE and PN+RAL+LE groups compared with the PN and PN+RAL groups (P < 0.01) and in the 4% and 13.5% PN+LE groups compared with PN alone. Hepatic total retinol was higher in the RAL-fed mice (P < 0.0001), but RAL did not alter TG mass. mRNA transcripts for fatty acid synthase (Fasn) and sterol regulatory element-binding protein-1c (Srebpf1) were higher in the PN compared with the NC mice, but FAS protein and Srebpf1 mRNA were lower in the PN+LE groups compared with PN alone. The inflammation marker serum amyloid P component was also reduced. In summary, LE given either i.v. or orally may be sufficient to reduce the steatotic potential of orally fed high-dextrose formulas and may suppress the early development of HS during PN therapy.
authors: Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA.
authors: Kyoko
authors: K
authors: Ito
authors: Lei
authors: L
authors: Hao
authors: Amanda E
authors: AE
authors: Wray
authors: A Catharine
authors: AC
authors: Ross
mesh_terms: D000284:Administration, Oral; D000818:Animals; D004041:Dietary Fats / Q000494:pharmacology / Q000627:therapeutic use; D005217:Fat Emulsions, Intravenous / Q000494:pharmacology / Q000627:therapeutic use*; D064429:Fatty Acid Synthases / Q000235:genetics / Q000378:metabolism; D005234:Fatty Liver / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D005947:Glucose / Q000009:adverse effects; D007249:Inflammation / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010288:Parenteral Nutrition / Q000009:adverse effects*; D012333:RNA, Messenger / Q000378:metabolism; D012172:Retinaldehyde / Q000494:pharmacology / Q000627:therapeutic use; D000683:Serum Amyloid P-Component / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism*; D014801:Vitamin A / Q000097:blood
chemical_list: D004041:Dietary Fats; D005217:Fat Emulsions, Intravenous; D018836:Inflammation Mediators; D012333:RNA, Messenger; D000683:Serum Amyloid P-Component; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; D014801:Vitamin A; D064429:Fatty Acid Synthases; D005947:Glucose; D012172:Retinaldehyde