title: Effects of repeated boluses of sucrose on proliferation and on AOM-induced aberrant crypt foci in rat colon.
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.
authors.affiliation: Department of Pharmacology and Toxicology, University of Florence, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Luceri
authors.forename: G
authors.initials: G
authors.lastname: Caderni
authors.forename: L
authors.initials: L
authors.lastname: Lancioni
authors.forename: S
authors.initials: S
authors.lastname: Aiolli
authors.forename: P
authors.initials: P
authors.lastname: Dolara
authors.forename: V
authors.initials: V
authors.lastname: Mastrandrea
authors.forename: F
authors.initials: F
authors.lastname: Scardazza
authors.forename: G
authors.initials: G
authors.lastname: Morozzi
mesh_terms: D000818:Animals; D001397:Azoxymethane; D001647:Bile Acids and Salts / Q000378:metabolism; D002273:Carcinogens; D002455:Cell Division / Q000187:drug effects*; D003110:Colonic Neoplasms / Q000139:chemically induced* / Q000473:pathology*; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D007413:Intestinal Mucosa / Q000187:drug effects / Q000473:pathology; D009077:Mucins / Q000096:biosynthesis; D051381:Rats; D011916:Rats, Inbred F344; D052116:Sialomucins; D013213:Starch / Q000008:administration & dosage / Q000494:pharmacology; D013395:Sucrose / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D001647:Bile Acids and Salts; D002273:Carcinogens; D005227:Fatty Acids; D009077:Mucins; D052116:Sialomucins; D013395:Sucrose; D013213:Starch; D001397:Azoxymethane