Colonic mucosal proliferation, aberrant crypt foci (ACF) induction, and fecal bile acids, parameters connected to the risk of colon cancer development, were studied in female F344 rats treated with starch or sucrose boluses or with a sucrose diet. Cell proliferation was higher in animals treated with a single sucrose bolus than in those given a starch bolus (15 g/kg body wt), with 4.3 +/- 0.64 and 2.17 +/- 0.57 (SE) mitotic figures (MF) per crypt in the sucrose and starch bolus groups, respectively (p < 0.01). When azoxymethane (AOM, 20 mg/kg) was administered 24 hours after a single sucrose or starch bolus, the number of ACF per colon after 30 days was higher in the sucrose bolus group [107.5 +/- 9.5 (SE)] than in the starch bolus group (67.8 +/- 0.9, p < 0.01). In additional experiments, colon cell proliferation (MF/crypt) was higher in rats given boluses of sucrose three times per week for 40 days after AOM (20 mg/kg) [5.9 +/- 0.7 (SE)] than in rats given starch boluses (2.96 +/- 0.4) or fed sucrose continuously (3.6 +/- 0.5). On the contrary, after 40 days of dietary treatment, the number, dimension, and percentage of ACF secreting sulfomucins and sialomucins were not varied among these three groups. However, the percentage of "large ACF" (ACF with > or = 4 crypts) secreting sialomucins or predominantly sialomucins was higher (p < 0.05) in the sucrose bolus group than in the starch group. The concentration of fecal bile acids and long-chain fatty acids was the same in the sucrose and starch groups, but the concentrations of deoxycholic and oleic acid were significantly higher in the sucrose bolus group. In conclusion, the administration of sucrose as a bolus had a stronger effect than continuous sucrose feeding on some parameters related to colon carcinogenesis and might be considered a risk factor in colon carcinogenesis.

Effects of repeated boluses of sucrose on proliferation and on AOM-induced aberrant crypt foci in rat colon / C. Luceri; G. Caderni; L. Lancioni; S. Aiolli; P. Dolara; V. Mastrandrea; F. Scardazza; G. Morozzi. - In: NUTRITION AND CANCER. - ISSN 0163-5581. - STAMPA. - 25:(1996), pp. 187-196.

Effects of repeated boluses of sucrose on proliferation and on AOM-induced aberrant crypt foci in rat colon

LUCERI, CRISTINA;CADERNI, GIOVANNA;DOLARA, PIERO;
1996

Abstract

Colonic mucosal proliferation, aberrant crypt foci (ACF) induction, and fecal bile acids, parameters connected to the risk of colon cancer development, were studied in female F344 rats treated with starch or sucrose boluses or with a sucrose diet. Cell proliferation was higher in animals treated with a single sucrose bolus than in those given a starch bolus (15 g/kg body wt), with 4.3 +/- 0.64 and 2.17 +/- 0.57 (SE) mitotic figures (MF) per crypt in the sucrose and starch bolus groups, respectively (p < 0.01). When azoxymethane (AOM, 20 mg/kg) was administered 24 hours after a single sucrose or starch bolus, the number of ACF per colon after 30 days was higher in the sucrose bolus group [107.5 +/- 9.5 (SE)] than in the starch bolus group (67.8 +/- 0.9, p < 0.01). In additional experiments, colon cell proliferation (MF/crypt) was higher in rats given boluses of sucrose three times per week for 40 days after AOM (20 mg/kg) [5.9 +/- 0.7 (SE)] than in rats given starch boluses (2.96 +/- 0.4) or fed sucrose continuously (3.6 +/- 0.5). On the contrary, after 40 days of dietary treatment, the number, dimension, and percentage of ACF secreting sulfomucins and sialomucins were not varied among these three groups. However, the percentage of "large ACF" (ACF with > or = 4 crypts) secreting sialomucins or predominantly sialomucins was higher (p < 0.05) in the sucrose bolus group than in the starch group. The concentration of fecal bile acids and long-chain fatty acids was the same in the sucrose and starch groups, but the concentrations of deoxycholic and oleic acid were significantly higher in the sucrose bolus group. In conclusion, the administration of sucrose as a bolus had a stronger effect than continuous sucrose feeding on some parameters related to colon carcinogenesis and might be considered a risk factor in colon carcinogenesis.
1996
25
187
196
C. Luceri; G. Caderni; L. Lancioni; S. Aiolli; P. Dolara; V. Mastrandrea; F. Scardazza; G. Morozzi
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Utilizza questo identificatore per citare o creare un link a questa risorsa: https://hdl.handle.net/2158/253293
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