The effects of exogenous insulin-like growth factor-I (IGF-I) on colonic adaptation were examined in male Sprague-Dawley rats (n = 60, 225-275 mg) after either a 60% small bowel and cecal resection (RX) or mid-small bowel transection with reanastomosis (TX). Animals received a 7-day treatment with either IGF-I (2.4 mg.kg-1.day-1) or vehicle (V; 0.1 mol/l acetic acid). Body weight decreased significantly after resection (-25.6 +/- 4.0 g; P < 0.05 vs. TX/V). IGF-I treatment significantly reduced weight loss after resection (-12.4 +/- 3.8 g; P < 0.01 vs. RX/V) and induced significant weight gain after transection (15.6 +/- 4.0 g; P < 0.05 vs. TX/V). Plasma IGF-I decreased with resection (526 +/- 41 TX/V vs. 344 +/- 17 ng/ml RX/V; P < 0.01). IGF-I treatment significantly increased plasma IGF-I levels (805 +/- 100 ng/ml TX/IGF, 677 +/- 56 ng/ml RX/IGF). After resection, IGF-I treatment significantly increased colonic mucosal weight, DNA, protein content, and crypt depth when compared with resection alone (P < 0.05). Colonic water absorption, measured by an in vivo [3H]polyethylene glycol assay, was significantly increased by IGF-I treatment in resected animals (399 +/- 23 RX/IGF vs. 306 +/- 32 microliter.cm-1.h-1 RX/V; P < 0.05). Resection resulted in increased steady-state colonic IGF-I mRNA (182% of TX/V; P < 0.01) without significantly affecting IGF-I receptor mRNA expression. Regulation of IGF binding protein (BP)-3 and -4 was discoordinate, with IGFBP-3 mRNA tending to decrease with resection (67% of TX/V; P is not significant) and IGFBP-4 increasing significantly (191% of TX/V; P < 0.05). An important role for IGF-I in colonic adaptation after massive intestinal resection is indicated by 1) significantly enhanced colonic mucosal growth and water absorption with IGF-I treatment and 2) postresection upregulation of colonic IGF-I mRNA and alteration of IGFBP-3 and IGFBP-4 mRNA expression.

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Colonic infusion of short chain fatty acids (SCFAs) is trophic to rat jejunum and is associated with raised jejunal gastrin concentration. This study examined the hypothesis that the jejunal trophic effects of colonic SCFAs are mediated in part by gastrin. Forty six adult rats underwent caecectomy to reduce endogenous production of SCFA, ileocolonic anastomosis, and placement of a colonic infusion catheter. SCFA (70 mM acetate, 35 mM propionate, 20 mM butyrate) or saline were continuously infused into the colon for seven days. Rats received either a gastrin receptor blocker (L-365,260) or a control solution and animals were killed on day 8. SCFA infused into the colon acted systemically to significantly improve jejunal structure and increase jejunal gastrin concentrations. Gastrin receptor blockade abolished effects of SCFA on jejunal DNA, protein, crypt cell proliferation, and gastrin. Gastrin blockade did not reduce SCFA induced augmentation of villous height or crypt depth. It is concluded that the jejunal trophic effects of colonically infused SCFA are mediated in part by gastrin. (Gut1995;37:81-86)