title: Resistant starches protect against colonic DNA damage and alter microbiota and gene expression in rats fed a Western diet.
abstract: Resistant starch (RS), fed as high amylose maize starch (HAMS) or butyrylated HAMS (HAMSB), opposes dietary protein-induced colonocyte DNA damage in rats. In this study, rats were fed Western-type diets moderate in fat (19%) and protein (20%) containing digestible starches [low amylose maize starch (LAMS) or low amylose whole wheat (LAW)] or RS [HAMS, HAMSB, or a whole high amylose wheat (HAW) generated by RNA interference] for 11 wk (n = 10/group). A control diet included 7% fat, 13% protein, and LAMS. Colonocyte DNA single-strand breaks (SSB) were significantly higher (by 70%) in rats fed the Western diet containing LAMS relative to controls. Dietary HAW, HAMS, and HAMSB opposed this effect while raising digesta levels of SCFA and lowering ammonia and phenol levels. SSB correlated inversely with total large bowel SCFA, including colonic butyrate concentration (R(2) = 0.40; P = 0.009), and positively with colonic ammonia concentration (R(2) = 0.40; P = 0.014). Analysis of gut microbiota populations using a phylogenetic microarray revealed profiles that fell into 3 distinct groups: control and LAMS; HAMS and HAMSB; and LAW and HAW. The expression of colonic genes associated with the maintenance of genomic integrity (notably Mdm2, Top1, Msh3, Ung, Rere, Cebpa, Gmnn, and Parg) was altered and varied with RS source. HAW is as effective as HAMS and HAMSB in opposing diet-induced colonic DNA damage in rats, but their effects on the large bowel microbiota and colonocyte gene expression differ, possibly due to the presence of other fiber components in HAW.
authors.affiliation: CSIRO Preventative Health, Adelaide, South Australia, Australia.
authors.forename: Michael A
authors.initials: MA
authors.lastname: Conlon
authors.forename: Caroline A
authors.initials: CA
authors.lastname: Kerr
authors.forename: Christopher S
authors.initials: CS
authors.lastname: McSweeney
authors.forename: Robert A
authors.initials: RA
authors.lastname: Dunne
authors.forename: Janet M
authors.initials: JM
authors.lastname: Shaw
authors.forename: Seungha
authors.initials: S
authors.lastname: Kang
authors.forename: Anthony R
authors.initials: AR
authors.lastname: Bird
authors.forename: Matthew K
authors.initials: MK
authors.lastname: Morell
authors.forename: Trevor J
authors.initials: TJ
authors.lastname: Lockett
authors.forename: Peter L
authors.initials: PL
authors.lastname: Molloy
authors.forename: Ahmed
authors.initials: A
authors.lastname: Regina
authors.forename: Shusuke
authors.initials: S
authors.lastname: Toden
authors.forename: Julie M
authors.initials: JM
authors.lastname: Clarke
authors.forename: David L
authors.initials: DL
authors.lastname: Topping
mesh_terms: D000688:Amylose / Q000494:pharmacology; D000821:Animal Feed; D000818:Animals; D001419:Bacteria / Q000187:drug effects* / Q000254:growth & development; D003106:Colon / Q000382:microbiology* / Q000502:physiology*; D015179:Colorectal Neoplasms / Q000453:epidemiology / Q000235:genetics / Q000517:prevention & control*; D004249:DNA Damage / Q000502:physiology*; D004040:Dietary Carbohydrates / Q000494:pharmacology; D004043:Dietary Fiber / Q000494:pharmacology; D004044:Dietary Proteins / Q000494:pharmacology; D015870:Gene Expression / Q000502:physiology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects / Q000502:physiology; D008297:Male; D054892:Metagenome / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D013213:Starch / Q000494:pharmacology*; D003313:Zea mays
chemical_list: D004040:Dietary Carbohydrates; D004043:Dietary Fiber; D004044:Dietary Proteins; D013213:Starch; D000688:Amylose