BACKGROUND/AIMS: Remnant small intestine undergoes adaptation following massive resection. The aim of this study was to examine the effect of epidermal growth factor (EGF) on ileal adaptation following proximal resection. METHODS: New Zealand white rabbits, aged 8 weeks, underwent 2/3 proximal resection, and ileal mucosal adaptation was assessed 10 and 21 days postsurgery. In a second series of experiments, animals with resection received oral EGF (40 micrograms.kg-1.day-1) for 5 days, and the effect on adaptation was assessed 10 days postsurgery. RESULTS: Transection alone stimulated mucosal hyperplasia, intestinal sucrase specific activity, and glucose transport at 10 days but not at 21 days. Resection resulted in mucosal hyperplasia at both time periods and increased disaccharidase specific activity at 10 days postresection. In contrast, 3 O-methyl-D-glucose transport was significantly decreased compared with both groups at both time periods. EGF treatment in animals with resection did not alter mucosal proliferation but did stimulate maltase specific activity and caused a 3-4-fold increase in glucose transport and phlorizin binding. CONCLUSIONS: Following proximal resection, adaptation of intestinal digestive and absorptive function does not parallel mucosal hyperplasia. Administration of EGF to resected animals enhances glucose absorption and may have a therapeutic role in the management of short gut syndrome.
BACKGROUND/AIMS: Remnant small intestine undergoes adaptation following massive resection. The aim of this study was to examine the effect of epidermal growth factor (EGF) on ileal adaptation following proximal resection. METHODS: New Zealand white rabbits, aged 8 weeks, underwent 2/3 proximal resection, and ileal mucosal adaptation was assessed 10 and 21 days postsurgery. In a second series of experiments, animals with resection received oral EGF (40 micrograms.kg-1.day-1) for 5 days, and the effect on adaptation was assessed 10 days postsurgery. RESULTS: Transection alone stimulated mucosal hyperplasia, intestinal sucrase specific activity, and glucose transport at 10 days but not at 21 days. Resection resulted in mucosal hyperplasia at both time periods and increased disaccharidase specific activity at 10 days postresection. In contrast, 3 O-methyl-D-glucose transport was significantly decreased compared with both groups at both time periods. EGF treatment in animals with resection did not alter mucosal proliferation but did stimulate maltase specific activity and caused a 3-4-fold increase in glucose transport and phlorizin binding. CONCLUSIONS: Following proximal resection, adaptation of intestinal digestive and absorptive function does not parallel mucosal hyperplasia. Administration of EGF to resected animals enhances glucose absorption and may have a therapeutic role in the management of short gut syndrome.