title: Enteral administration of high-fat nutrition before and directly after hemorrhagic shock reduces endotoxemia and bacterial translocation.
abstract: OBJECTIVE
  To determine whether potential enhancement of endotoxin neutralization via high-fat enteral nutrition affects endotoxemia and bacterial translocation after hemorrhage.
  
  
  BACKGROUND
  Endotoxin and bacterial translocation due to gut barrier failure are important initiating events in the pathogenesis of sepsis after hemorrhage. Systemic inhibition of endotoxin activity attenuates bacterial translocation and distant organ damage. Triacylglycerol-rich lipoproteins constitute a physiological means of binding and neutralizing endotoxin effectively. We hypothesized that enhancement of triacylglycerol-rich lipoproteins via high-fat enteral nutrition would reduce endotoxemia and prevent bacterial translocation.
  
  
  METHODS
  A rat model of nonlethal hemorrhagic shock was used. Hemorrhagic shock (HS) rats were divided into 3 groups: rats starved overnight (HS-S); rats fed with a low-fat enteral diet (HS-LF), and rats receiving a high-fat enteral diet (HS-HF).
  
  
  RESULTS
  Circulating triacylglycerol and apolipoprotein B, reflecting the amount of triacylglycerol-rich lipoproteins, were elevated in HS-HF rats compared with both HS-S rats (P <or= 0.005 and P <or= 0.05, respectively) and HS-LF rats (P <or= 0.005 and P <or= 0.05). Circulating endotoxin was lower in HS-HF rats (7.2 +/- 10.2 pg/ml) compared with both HS-S rats (29.1 +/- 13.4 pg/ml, P <or= 0.005) and HS-LF rats (29.9 +/- 5.2 pg/ml, P <or= 0.005). In line, bacterial translocation was lower in HS-HF rats (incidence 4/8 rats; median 3 [range 0-144] cfu/g) compared with both HS-S rats (8/8; 212 [60-483] cfu/g; P = 0.006), and HS-LF rats (8/8; 86 [30-209] cfu/g; P = 0.002).
  
  
  CONCLUSIONS
  This study is the first to show that high-fat enteral nutrition, leading to increased plasma triacylglycerol and apolipoprotein B levels, significantly decreases endotoxemia and bacterial translocation after hemorrhage.
authors.affiliation: Department of Surgery, University of Maastricht and University Hospital Maastricht, the Netherlands.
authors.forename: Misha D P
authors.initials: MD
authors.lastname: Luyer
authors.forename: Jan A
authors.initials: JA
authors.lastname: Jacobs
authors.forename: Anita C E
authors.initials: AC
authors.lastname: Vreugdenhil
authors.forename: M'hamed
authors.initials: M
authors.lastname: Hadfoune
authors.forename: Cornelis H C
authors.initials: CH
authors.lastname: Dejong
authors.forename: Wim A
authors.initials: WA
authors.lastname: Buurman
authors.forename: Jan Willem M
authors.initials: JW
authors.lastname: Greve
mesh_terms: D000818:Animals; D001055:Apolipoproteins B / Q000097:blood; D018988:Bacterial Translocation; D004041:Dietary Fats / Q000008:administration & dosage*; D004731:Endotoxins / Q000097:blood*; D004750:Enteral Nutrition; D008099:Liver / Q000382:microbiology; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D008643:Mesentery; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000097:blood* / Q000382:microbiology*; D013154:Spleen / Q000382:microbiology; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D004041:Dietary Fats; D004731:Endotoxins; D014280:Triglycerides