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Glucagon-like Peptide-2 (GLP-2) Response to Enteral Intake in Children During Anti-Cancer Treatment

Andreassen, B. U.*; Pærregaard, A.†; Schmiegelow, K.‡; Rechnitzer, C.‡; Heilman, C.‡; Hartmann, B.§; Holst, J. J.§; Michaelsen, K. F.*¶

Journal of Pediatric Gastroenterology & Nutrition: January 2005 - Volume 40 - Issue 1 - pp 48-53
Original Articles: Hepatology and Nutrition

Background: Intestinal dysfunction is frequent in cancer and during anti-cancer treatment. Glucagon-like peptide-2 (GLP-2) is secreted in a nutrition-dependent manner from the intestinal enteroendocrine L-cells. It accelerates crypt cell proliferation and nutrient absorption, inhibits enterocyte apoptosis and decreases mucosal permeability. Lack of GLP-2 may increase the risk of malabsorption and intestinal bacterial translocation. The aim of this study is to evaluate meal stimulated secretion of GLP-2 in children with cancer undergoing anti-cancer treatment.

Methods: Plasma-GLP-2 analysis after an overnight fast and 1 hour after intake of a mixed test meal. Data on gastrointestinal toxicity, blood neutrophile counts and food records were included in the analysis.

Results: Forty-four meal stimulation tests were performed in 25 children (median age, 6.0 years; range, 2.5-19) during anti-cancer treatment. Median GI toxicity score was 5 (range, 0-15), and mean energy intake was 62.4% of recommended values. P-GLP-2 values increased from mean (SD) 38 (18) to 63 (51) pmol/l (P < 0.0001). Twelve of the meal stimulation tests (28%) resulted in a p-GLP-2 increase >2 fold, which is assumed to be the lower limit of normal values. The increase was strongly dependent on the energy intake (r = 0.62, P < 0.0001), while toxicity score and neutrophile count had no significant influence (multiple regression).

Conclusion: In children treated with anti-cancer therapy, GLP-2 secretion seems to be normal if the enteral energy intake is sufficient. Insufficient GLP-2 secretion could influence the gastrointestinal problems seen in the children with a low enteral energy intake.

*Paediatric Nutrition Unit, †Section of Paediatrics, Hvidovre Hospital; ‡Paediatric Clinic II, Rigs-hospital; §Department of Medical Physiology, Panum Institute, Copenhagen; ¶Department of Human Nutrition, The Royal Veterinary and Agricultural University, Frederiksberg, Denmark

This study was supported financial by The Danish Child Cancer Foundation, Dagmar Marshall Foundation, Rosalie Petersen Foundation, Mimi and Victor Larsen's Foundation, grocer Kristian and Margrethe Kjær Foundation, manufacturer Einar Willumsen's Foundation, The Frænkel's Foundation and AP Møller and Chastine Mc-Kinney Møller's Foundation, which had no economical interests in the project.

Address correspondence and reprint requests to Dr. Bente Utoft Andreassen, Paediatric Nutrition Unit, Section 4094, Juliane Marie Centre, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen (e-mail:

© 2005 Lippincott Williams & Wilkins, Inc.