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Gastroenterology Research and Practice
Volume 2013 (2013), Article ID 814054, 4 pages
Research Article

Oral Glutamine Supplement Inhibits Ascites Formation in Peritoneal Carcinomatosis Mouse Model

1Division of Gastroenterology, Department of Internal Medicine, Mackay Memorial Hospital, Taiwan
2Mackay Junior College of Medicine, Nursing and Management, Taipei, Taiwan
3Mackay Medical College, New Taipei, Taiwan
4Department of Radiation Oncology, Mackay Memorial Hospital, Taipei, Taiwan
5Graduate Institute of Pharmacology, Taipei Medical University, Taipei, Taiwan

Received 12 July 2013; Accepted 12 September 2013

Academic Editor: Antoni Castells

Copyright © 2013 Ming-Jen Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Peritoneal carcinomatosis (PC) accompanied with ascites formation causes several distressing symptoms, resulting in poor quality of life. Methods. Twenty BALB/c nude mice generated by direct orthotopic injection of human pancreatic cancer PANC-1 cells were randomized to receive either a stock laboratory diet or a stock diet supplemented with glutamine. Half of the mice were sacrificed at day 76 to measure the amount of ascitic fluid and pancreatic tumor volume. The remaining mice were subject to survival analysis. Serum albumin levels were estimated every 2 weeks. Results. At day 76, the average amount of ascitic fluid measured in the control group was  mL compared to  mL from the glutamine-supplemented mice ( ). The volume of pancreatic tumor was  cm3 in the control group and  cm3 in glutamine-supplemented mice ( ). The mean survival time of glutamine-supplemented mice was prolonged from to days ( ). Mean serum albumin levels were higher in the glutamine-supplemented group. Conclusions. This preclinical study showed that oral supplementation of glutamine may provide ascites-reducing activity in pancreatic cancer patients with PC, via a cell-mediated immunity-independent mechanism.