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Novel effect of glucagon-like peptide-2 for hepatocellular injury in a parenterally fed rat model of short bowel syndrome.
Pediatr Surg Int. 2019 Dec; 35(12):1345-1351.PS

Abstract

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.

Authors+Show Affiliations

Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan. Clinical Training Center, Kagoshima University Hospital, Kagoshima, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan. sieiri@m.kufm.kagoshima-u.ac.jp.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31555865

Citation

Yano, Keisuke, et al. "Novel Effect of Glucagon-like Peptide-2 for Hepatocellular Injury in a Parenterally Fed Rat Model of Short Bowel Syndrome." Pediatric Surgery International, vol. 35, no. 12, 2019, pp. 1345-1351.
Yano K, Kaji T, Onishi S, et al. Novel effect of glucagon-like peptide-2 for hepatocellular injury in a parenterally fed rat model of short bowel syndrome. Pediatr Surg Int. 2019;35(12):1345-1351.
Yano, K., Kaji, T., Onishi, S., Machigashira, S., Nagai, T., Harumatsu, T., Yamada, K., Yamada, W., Muto, M., Nakame, K., Mukai, M., & Ieiri, S. (2019). Novel effect of glucagon-like peptide-2 for hepatocellular injury in a parenterally fed rat model of short bowel syndrome. Pediatric Surgery International, 35(12), 1345-1351. https://doi.org/10.1007/s00383-019-04560-8
Yano K, et al. Novel Effect of Glucagon-like Peptide-2 for Hepatocellular Injury in a Parenterally Fed Rat Model of Short Bowel Syndrome. Pediatr Surg Int. 2019;35(12):1345-1351. PubMed PMID: 31555865.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Novel effect of glucagon-like peptide-2 for hepatocellular injury in a parenterally fed rat model of short bowel syndrome. AU - Yano,Keisuke, AU - Kaji,Tatsuru, AU - Onishi,Shun, AU - Machigashira,Seiro, AU - Nagai,Taichiro, AU - Harumatsu,Toshio, AU - Yamada,Koji, AU - Yamada,Waka, AU - Muto,Mitsuru, AU - Nakame,Kazuhiko, AU - Mukai,Motoi, AU - Ieiri,Satoshi, Y1 - 2019/09/25/ PY - 2019/9/12/accepted PY - 2019/9/27/pubmed PY - 2020/2/13/medline PY - 2019/9/27/entrez KW - Glucagon-like peptide-2 KW - IFALD KW - NAFLD KW - Short bowel syndrome KW - Steatosis KW - Total parenteral nutrition SP - 1345 EP - 1351 JF - Pediatric surgery international JO - Pediatr Surg Int VL - 35 IS - 12 N2 - 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. SN - 1437-9813 UR - https://www.unboundmedicine.com/medline/citation/31555865/Novel_effect_of_glucagon_like_peptide_2_for_hepatocellular_injury_in_a_parenterally_fed_rat_model_of_short_bowel_syndrome_ DB - PRIME DP - Unbound Medicine ER -