The management of patients with the short bowel syndrome

Table 3 Molecules that regulate intestinal adaptation

Molecule	Effect on Intestinal Adaptation
Glucagon-Like	Treatment of rats with a 75% mid small bowel resection with twice daily injections of 0.1ìg per gram of bodyweight for 21 d induced led to
Peptide 2	mucosal hyperplasia in the proximal jejunum but not in the terminal ileum and a significant increase in intestinal absorptive capacity[50].
Interleukin-11	Treatment of rats with a 90% small bowel resectionwith twice daily injections of 125 mg·g-1ªª Il-11 significantly increasedvillus height and crypt
	cell mitotic rates[51].
Keratinocyte Growth	Treatment of rats with a 75% small bowel resection with 3 mg·kg-1·d-1 of KGF enhanced intestinal adaptation as assessed by mucosal
Factor (KGF)	cellularity, and biochemical activity in duodenal, jejunal and ileal segments[52].
Transforming factor-α	Treatment of mice with a 50% small bowel resection with intraperitoneal TGF-α enhanced intestinal adaptation[53].
Growth Hormone	Treatment of rats with a 75% small intestinal resection with 0.1 mg·kg-1·kg-1·2 d-1 d for 28 d enhanced ileal adaptation as assessed by ileal
	mucosal height. Treatment with growth hormone did not alter ileal mucosal DNA content or ileal mucosal IGF-1 content[54].
	Treatment of rats with an 80% jejunoileal resection with synthetic rat GH for up to 14 d did not enhance ileal adaptation[55].
	Treatment of an infant with only 25 cm of jejunum and 2 cm of ileum, with an ileocecal valve, with a 4-week course of 0.5 U/kg of GH
	allowing wean ing from TPN[56].
	Ten patients with short bowel syndrome were treated with daily subcutaneous doses of recombinant human GH (rhGH) of 0.024 mg·kg-1·d-1 or a placebo for 8 wk in a crossover cli nical trial that included a wash-out period of at least 12 wk. Low-dose rhGH doubled serum levels
	of IGF-1 and increased body weight and lean body mass; but there were no significant changes in absorptive capacity of water, energy, or protein[57].
Insulin-like	Treatment of rats with 70% and 80% jejuno-ileal resection with IGF-1 or analogues significantly attenuated malabsorption of fat and
Growth Factor-1	increased weight of stomach and proximal small bowel[58].
	Gastrostomy-fed rats underwent 80% jejuno-ileal resection followed by infusion of 2.4mg·kg-1·d-1 IGF-1 for 7 d. IGF-1 infusion led to a
	modest increase in ileal but not jejunal growth[15].
	Treatment of TPN-fed rats for 7 d with IGF-1 after a 60% jejunoileal resection led to an increase in jejunal mass, enterocyte proliferation and
	migration rates yet had minimal effect on colonic structure[59].
Epidermal Growth	Treatment of rabbits with 2/3 proximal resection with oral EGF (40 µg·kg-1·d-1) for 5 d led to an increase in maltase specific activity and a 3
Factor (EGF)	-4 fold increase in glucose transport and phlorizin binding[60].
	Treatment of rabbits with a 50%-60% small bowel resection with 0.3 µg·kg-1·h-1 for 7 d led to a foufold increase in mucosal dryweight at 3
	wk post-resection[61].
	Treatment of rats with a 75% small bowel resection with 6.25 µg·kg-1·h-1 of EGF increased mucosal thickness at 28 d post-resection[62].
Neurotensin	Treatment of rats with a 75% small bowel resection with 600 µg·kg-1·d-1 led to an increase in the rate of mucosal proliferation[63].