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Purpose: Total parental nutrition (TPN) causes gastrointestinal mucosal atrophy. The present study investigated the effects of hepatocyte growth factor (HGF) on the intestinal mucosal atrophy induced by TPN. Methods: Rats underwent jugular vein catheterization and were divided into four groups: oral feeding (OF), TPN alone (TPN), TPN plus low-dose HGF (0.3 mg/kg/day; TPNLH), and TPN plus high-dose HGF (1.0 mg/kg/day; TPNHH). On day 7, rats were euthanized, and the small intestine was harvested and evaluated histologically. The expression of c-MET, a receptor of HGF, and nutrition transporter protein were evaluated using quantitative polymerase chain reaction. Results: The jejunal villus height (VH) and absorptive mucosal surface area in the TPNHH group were significantly higher than in the TPN group (p < 0.05). The VH in the ileum showed the same trend only in the TPNHH group, albeit without statistical significance. The crypt cell proliferation rate (CCPR) of the jejunum in both HGF-treated groups was significantly higher than in the TPN group (p < 0.01). The expression of c-MET and transporter protein in all TPN-treated groups was decreased compared with that in the OF group. Conclusion: HGF attenuated TPN-associated intestinal mucosal atrophy by increasing the villus height, which was associated with an increase in CCPR. [ABSTRACT FROM AUTHOR]

Purpose: Total parenteral nutrition (TPN) sometimes induces parenteral nutrition-associated liver disease (PNALD). Hepatocyte growth factor (HGF) acts as a potent hepatocyte mitogen anti-inflammatory and antioxidant actions. We aimed to evaluate the effect of HGF on PNALD in a rat model of TPN. Methods: A catheter was placed in the right jugular vein for 7-day continuous TPN. All rats were divided into three groups: TPN alone (TPN group), TPN plus intravenous HGF at 0.3 mg/kg/day [TPN + HGF (low) group], and TPN plus HGF at 1.0 mg/kg/day [TPN + HGF (high) group]. On day 7, livers were harvested and the histology, inflammatory cytokines and apoptosis were evaluated. Results: Histologically, lipid droplets were apparent in the TPN group, but decreased in the TPN + HGF (low) and TPN + HGF (high) groups. The histological nonalcoholic fatty liver disease activity scores in the TPN + HGF (low) and TPN + HGF (high) groups were significantly lower than that in the TPN group (p < 0.01). There were no significant differences in the inflammatory cytokine levels of the three groups. The caspase-9 expression levels in the TPN + HGF (low) and TPN + HGF (high) groups were significantly decreased in comparison to that in the control group (p < 0.05). Conclusion: The intravenous administration of HGF attenuated hepatic steatosis induced by 7-day TPN dose dependently. [ABSTRACT FROM AUTHOR]

Purpose: Composite lipid emulsion (CLE) has been used for intestinal failure-associated liver disease (IFALD) to compensate for the disadvantages of soybean oil lipid emulsion (SOLE) or fish oil lipid emulsion (FOLE). However, the influence of its administration is unclear. We evaluated the effects of these emulsions on IFALD using a rat model of the short-bowel syndrome. Methods: We performed jugular vein catheterization and 90% small bowel resection in Sprague–Dawley rats and divided them into four groups: control (C group), regular chow with intravenous administration of saline; and total parenteral nutrition co-infused with SOLE (SOLE group), CLE (CLE group) or FOLE (FOLE group). Results: Histologically, obvious hepatic steatosis was observed in the SOLE and CLE groups but not the FOLE group. The liver injury grade of the steatosis and ballooning in the FOLE group was significantly better than in the SOLE group (p < 0.05). The TNF-α levels in the liver in the FOLE group were significantly lower than in the SOLE group (p < 0.05). Essential fatty acid deficiency (EFAD) was not observed in any group. Conclusion: Fish oil lipid emulsion attenuated hepatic steatosis without EFAD, while CLE induced moderate hepatic steatosis. The administration of CLE requires careful observation to prevent PN-induced hepatic steatosis. [ABSTRACT FROM AUTHOR]