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  • Title: Ingestion of resistant starch protects endotoxin influx from the intestinal tract and reduces D-galactosamine-induced liver injury in rats.
    Author: Morita T, Tanabe H, Takahashi K, Sugiyama K.
    Journal: J Gastroenterol Hepatol; 2004 Mar; 19(3):303-13. PubMed ID: 14748878.
    Abstract:
    BACKGROUND AND AIMS: The aim of the present study was to examine the protective effect of a dietary high-amylose cornstarch (HAS) against D-galactosamine (D-GalN)-induced liver injury, focusing specifically on intestinal endotoxin translocation. METHODS: Male Wistar rats fed a HAS-free basal diet or a 30% HAS-supplemented diet were injected intraperitoneally with D-GalN. Serum transaminase activities, serum concentrations of tumor necrosis factor (TNF)-alpha, and portal venous endotoxin concentrations were determined at various time points. Ileal mucosal proliferation, small intestinal immunoglobulin (Ig)A and mucin, and the size of the cecal short-chain fatty acids (SCFA) pool were also determined. RESULTS: High-amylose cornstarch ingestion significantly reduced the increase in serum transaminase activities at 22 h after the injection of D-GalN. Rats fed the HAS diet showed a greater cecal SCFA production as measured by pool size than those fed the basal diet. Luminal IgA and mucin content were significantly greater in rats fed the HAS diet. Protein, DNA and RNA contents in the ileal mucosa were also higher in rats fed the 30% HAS diet. In a further experiment, portal venous endotoxin concentrations in rats fed the basal diet reached 72 ng/L at 4 h after D-GalN administration, but endotoxin was not detected in rats fed the HAS diet. At this time, portal endotoxin concentrations were significantly and positively correlated with the serum concentrations of TNF-alpha and serum alanine aminotransferase activities. CONCLUSION: These data support the view that HAS ingestion may reduce D-GalN-induced liver injury as a result of an inhibitory effect on endotoxin influx from the intestinal tract, at least in part as a result of alterations in the mucosal barrier functions.
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