PMID- 15113957
OWN - NLM
STAT- MEDLINE
DCOM- 20040610
LR  - 20230216
IS  - 0022-3166 (Print)
IS  - 0022-3166 (Linking)
VI  - 134
IP  - 5
DP  - 2004 May
TI  - Kupffer cell activity is involved in the hepatoprotective effect of dietary 
      oligofructose in rats with endotoxic shock.
PG  - 1124-9
AB  - In the present study, we tested the hypothesis that dietary oligofructose (FOS) 
      can modulate both the response to an endotoxic shock induced by 
      lipopolysaccharide (LPS) administration and the activity of resident hepatic 
      macrophages, i.e., Kupffer cells. Male Wistar rats (n = 5-9 per group) were fed a 
      standard diet or a diet supplemented with 10 g/100 g FOS for 3 wk. LPS (10 mg/kg) 
      or saline were injected i.p. after dietary treatment. After LPS injection, serum 
      levels of tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine, and 
      prostaglandin E(2) (PGE(2)), an immunosuppressive mediator, were higher in 
      FOS-treated rats than in control rats. Alanine aminotransferase (ALT) activity 
      was approximately 50% lower than in controls 24 h after LPS administration in 
      FOS-treated rats, suggesting less hepatic injury; this was confirmed through 
      histological analysis. FOS treatment increased the number of large phagocytic 
      Kupffer cells, as assessed by histological examination of the liver after 
      colloidal carbon injection into the portal vein. Precision-cut liver slices 
      (PCLS) from FOS-treated rats released more TNF-alpha and PGE(2) into the 
      incubation medium than PCLS from control rats, independently of LPS challenge in 
      vitro. This would suggest that the higher Kupffer cell phagocytic activity and 
      secretion capacity due to FOS supplementation improve LPS clearance in liver 
      tissue and reduce hepatocyte alterations. This study supports the hypothesis that 
      oligofructose might decrease liver tissue injury after endotoxic shock and 
      sepsis.
FAU - Neyrinck, Audrey M
AU  - Neyrinck AM
AD  - Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology, School of 
      Pharmacy, Universite Catholique de Louvain, B-1200 Brussels, Belgium.
FAU - Alexiou, Helene
AU  - Alexiou H
FAU - Delzenne, Nathalie M
AU  - Delzenne NM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Nutr
JT  - The Journal of nutrition
JID - 0404243
RN  - 0 (Blood Glucose)
RN  - 0 (Colloids)
RN  - 0 (Dietary Carbohydrates)
RN  - 0 (Enzymes)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Oligosaccharides)
RN  - 0 (Triglycerides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (oligofructose)
RN  - 7440-44-0 (Carbon)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Blood Glucose/analysis
MH  - Body Temperature/drug effects
MH  - Carbon/pharmacokinetics
MH  - Colloids
MH  - *Cytoprotection
MH  - Dietary Carbohydrates/*administration & dosage
MH  - Dinoprostone/blood
MH  - Enzymes/blood
MH  - In Vitro Techniques
MH  - Inflammation Mediators/metabolism
MH  - *Kupffer Cells
MH  - Lipopolysaccharides/pharmacology
MH  - Liver/*physiopathology
MH  - Male
MH  - Oligosaccharides/*administration & dosage
MH  - Rats
MH  - Rats, Wistar
MH  - Shock, Septic/*physiopathology
MH  - Triglycerides/blood
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2004/04/29 05:00
MHDA- 2004/06/21 10:00
CRDT- 2004/04/29 05:00
PHST- 2004/04/29 05:00 [pubmed]
PHST- 2004/06/21 10:00 [medline]
PHST- 2004/04/29 05:00 [entrez]
AID - S0022-3166(23)02771-2 [pii]
AID - 10.1093/jn/134.5.1124 [doi]
PST - ppublish
SO  - J Nutr. 2004 May;134(5):1124-9. doi: 10.1093/jn/134.5.1124.