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Purpose: The purpose of this study was to investigate the autophagy associated with apoptosis in hepatic damage in the short bowel syndrome rat model. Methods: SD rats underwent jugular vein catheterization for continuous total parenteral nutrition (TPN) and 90% small bowel resection. Animals were divided into two groups: TPN plus SBS (Control group) or TPN plus SBS plus intravenous administration of HGF (HGF group). On day 7, the rats were harvested, and hepatocellular injury was evaluated. Results: In an SBS rat model, hepatic steatosis and lobular inflammation were histologically suppressed in the HGF group (p < 0.01). The expression of tumor necrosis factor-α in the HGF group tend to be higher than that in the control group (p = 0.13). The gene expression of transforming Growth Factor-β in the HGF group was suppressed compared to the control group (p < 0.01). HGF treatment may have an antiapoptotic effect via the intrinsic pathway by caspase 9. Protein expressions of Rubicon (p = 0.03) and p62 (p < 0.01) in the HGF group were found to have increased compared to those in the control group. Conclusion: The inhibitory effect of HGF on hepatic steatosis remains unclear, and further studies focusing on the mechanisms of fat accumulation are needed. [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: Short bowel syndrome (SBS) patients require long-term parenteral nutrition following massive bowel resection, which causes intestinal failure-associated liver disease (IFALD). Previous reports have shown that glucagon-like peptide-2 (GLP-2) resulted in the bowel adaptation for SBS. The aim of this study was to evaluate the effect of GLP-2 for IFALD in a parenterally fed rat model.Methods: Using rat, a catheter was placed in the jugular vein, and 90% small bowel resection (SBR) was performed. Animals were divided into three groups: SBR and total parenteral nutrition (TPN) (SBS/TPN group), SBR and TPN plus GLP-2 at 1 µg/kg/h [SBS/TPN/GLP-2 (low) group], and SBR and TPN plus GLP-2 at 10 µg/kg/h [SBS/TPN/GLP-2 (high) group]. On day 13, the liver was harvested and analyzed by using nonalcoholic fatty liver disease (NAFLD) score.Results: Histologically, hepatic steatosis in the SBS/TPN group and SBS/TPN/GLP-2 (high) group was observed. Both steatosis and lobular inflammation score in the SBS/TPN/GLP-2 (low) group were significantly lower compared with those in the other two groups (p < 0.05). Active NAFLD score in the SBS/TPN/GLP-2 (low) group was significantly lower compared with that in the SBS/TPN/GLP-2 (high) group (p < 0.01).Conclusion: Low-dose GLP-2 intravenous administration improves hepatic steatosis of IFALD following in an SBS parenterally fed rat model. [ABSTRACT FROM AUTHOR]