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The administration of ghrelin improved hepatocellular injury following parenteral feeding in a rat model of short bowel syndrome.
Pediatr Surg Int. 2016 Dec; 32(12):1165-1171.PS

Abstract

PURPOSE

Long-term parenteral nutrition following massive bowel resection causes liver dysfunction, such as intestinal failure-associated liver disease (IFALD). IFALD includes two different states, cholestasis and steatosis, which represents a life-threatening complication. The previous reports have shown the protective role of ghrelin in the liver. The aim of this study was to evaluate the effects of the administration of ghrelin in the liver in a parenterally fed rat model of short bowel syndrome (SBS).

METHODS

Rats underwent jugular vein catheterization, and were divided into three groups: 90 % small bowel resection (90 % SBR) and TPN (SBS/TPN group), 90 % SBR and TPN plus ghrelin (SBS/TPN/ghrelin group), and sham operation with normal chow (sham group). Ghrelin was administered continuously at a dose of 10 μg/kg/day. On day 13, all rats were euthanized. The serum chemistry was analyzed, the lipid content of the liver was measured, and the liver tissue was histologically analyzed.

RESULT

The AST and LDH levels significantly increased, and the accumulation of lipids in the liver was observed in the TPN/SBS group. The accumulation of lipids in the liver of the rats in the SBS/TPN group was attenuated by the administration of ghrelin.

CONCLUSION

The administration of ghrelin has a therapeutic potential for IFALD.

Authors+Show Affiliations

Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.Department of Pathology and Oncology, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, Kagoshima, Japan.Department of Pathology and Oncology, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, Kagoshima, Japan.Department of Pathology, National Center for Children Health and Development, Tokyo, Japan.Department of Pathology and Oncology, Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area, Research and Education Assembly, Kagoshima University, Kagoshima, Japan.Department of Pediatric Surgery, Research Field in Medicine and Health Sciences, Medical and Dental Sciences 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

27651372

Citation

Onishi, Shun, et al. "The Administration of Ghrelin Improved Hepatocellular Injury Following Parenteral Feeding in a Rat Model of Short Bowel Syndrome." Pediatric Surgery International, vol. 32, no. 12, 2016, pp. 1165-1171.
Onishi S, Kaji T, Yamada W, et al. The administration of ghrelin improved hepatocellular injury following parenteral feeding in a rat model of short bowel syndrome. Pediatr Surg Int. 2016;32(12):1165-1171.
Onishi, S., Kaji, T., Yamada, W., Nakame, K., Moriguchi, T., Sugita, K., Yamada, K., Kawano, T., Mukai, M., Souda, M., Yamada, S., Yoshioka, T., Tanimoto, A., & Ieiri, S. (2016). The administration of ghrelin improved hepatocellular injury following parenteral feeding in a rat model of short bowel syndrome. Pediatric Surgery International, 32(12), 1165-1171.
Onishi S, et al. The Administration of Ghrelin Improved Hepatocellular Injury Following Parenteral Feeding in a Rat Model of Short Bowel Syndrome. Pediatr Surg Int. 2016;32(12):1165-1171. PubMed PMID: 27651372.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The administration of ghrelin improved hepatocellular injury following parenteral feeding in a rat model of short bowel syndrome. AU - Onishi,Shun, AU - Kaji,Tatsuru, AU - Yamada,Waka, AU - Nakame,Kazuhiko, AU - Moriguchi,Tomoe, AU - Sugita,Koushirou, AU - Yamada,Koji, AU - Kawano,Takafumi, AU - Mukai,Motoi, AU - Souda,Masakazu, AU - Yamada,Sohsuke, AU - Yoshioka,Takako, AU - Tanimoto,Akihide, AU - Ieiri,Satoshi, Y1 - 2016/09/20/ PY - 2016/09/13/accepted PY - 2016/9/22/pubmed PY - 2017/3/28/medline PY - 2016/9/22/entrez KW - Ghrelin KW - IFALD KW - NAFLD KW - Short bowel syndrome KW - Steatosis KW - Total parenteral nutrition SP - 1165 EP - 1171 JF - Pediatric surgery international JO - Pediatr Surg Int VL - 32 IS - 12 N2 - PURPOSE: Long-term parenteral nutrition following massive bowel resection causes liver dysfunction, such as intestinal failure-associated liver disease (IFALD). IFALD includes two different states, cholestasis and steatosis, which represents a life-threatening complication. The previous reports have shown the protective role of ghrelin in the liver. The aim of this study was to evaluate the effects of the administration of ghrelin in the liver in a parenterally fed rat model of short bowel syndrome (SBS). METHODS: Rats underwent jugular vein catheterization, and were divided into three groups: 90 % small bowel resection (90 % SBR) and TPN (SBS/TPN group), 90 % SBR and TPN plus ghrelin (SBS/TPN/ghrelin group), and sham operation with normal chow (sham group). Ghrelin was administered continuously at a dose of 10 μg/kg/day. On day 13, all rats were euthanized. The serum chemistry was analyzed, the lipid content of the liver was measured, and the liver tissue was histologically analyzed. RESULT: The AST and LDH levels significantly increased, and the accumulation of lipids in the liver was observed in the TPN/SBS group. The accumulation of lipids in the liver of the rats in the SBS/TPN group was attenuated by the administration of ghrelin. CONCLUSION: The administration of ghrelin has a therapeutic potential for IFALD. SN - 1437-9813 UR - https://www.unboundmedicine.com/medline/citation/27651372/The_administration_of_ghrelin_improved_hepatocellular_injury_following_parenteral_feeding_in_a_rat_model_of_short_bowel_syndrome_ DB - PRIME DP - Unbound Medicine ER -