Resistant starch modifies gut microflora and microbial metabolism in human flora-associated rats inoculated with faeces from Italian and UK donors

Silvi, Stefania; Rumney, Corinne; Cresci, Alberto; Rowland, I.R.

doi:10.1046/j.1365-2672.1999.00696.x

Cited by 196 publications

(124 citation statements)

References 39 publications

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“…RS has prebiotic properties. 36,37 Previous studies in rats have shown that as little as 10% HAS in the diet is capable of stimulating the production of desirable bacterial species like lactobacilli and bifidobacteria. 21 RS in the current study was able to induce positive changes in the luminal microenvironment such as acidification of digesta and increased faecal bulk both which may contribute to enhanced colonic health for the host.…”

Section: Discussionmentioning

confidence: 99%

Suppression of azoxymethane-induced colon cancer development in rats by dietary resistant starch

Leu¹,

Brown²,

Ying³

et al. 2007

Cancer Biology & Therapy

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Resistant starch is a complex carbohydrate that reaches the colon where it can be fermented by the colonic microflora resulting in production of short chain fatty acids (SCFA), in particular butyrate. RS effects on colorectal tumorigenesis are contrasting and protection remains controversial. Butyrate has an important role as the preferred metabolic fuel and regulator of colonocyte proliferation, differentiation and apoptosis and may play a role in cancer prevention. Thus variation in butyrate production from different substrates might explain the variation in effect of RS. This study evaluated the hypothesis that feeding dietary resistant starch (as high amylose maize starch) would protect against azoxymethane (AOM)-colon carcinogenesis and favorably influence the colonic luminal environment. Male Sprague-Dawley rats (n = 90) were provided one of three diets: Control (without added dietary fibre or RS), 10% HAS (contained 100 g/kg raw high amylose maize starch) or 20% HAS (contained 200 g/kg high amylose maize starch). Rats were fed their experimental diets for four weeks after which they were injected with AOM (15 mg/kg) during the fifth and six week. Colons were resected (25 weeks post second injection) for evaluation of tumor formation, apoptosis, proliferating cell nuclear antigen (PCNA) labelling index and short chain fatty acid levels. Feeding resistant starch significantly reduced the incidence (p < 0.01) and multiplicity (p < 0.05) of adenocarcinomas in the colon compared to the Control diet. Both doses of HAS resulted in similar protection against colon tumorigenesis. Feeding RS significantly increased total SCFA concentrations, including butyrate in the distal colon. Apoptosis (p < 0.01) was also enhanced while PCNA labelling index was reduced (p < 0.01) in the distal colon with resistant starch feeding. The protective effect of consumption of RS as dietary high-amylose cornstarch against colon cancer development appears to be related to active fermentation in the colon, particularly through production of butyrate.

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Section: Discussionmentioning

confidence: 99%

Suppression of azoxymethane-induced colon cancer development in rats by dietary resistant starch

Leu¹,

Brown²,

Ying³

et al. 2007

Cancer Biology & Therapy

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“…In a similarly designed study, chronic ingestion of FOS did not improve GI tolerance or reduce breath hydrogen excretion in healthy subjects (Briet et al, 1995). Although adaptive metabolic changes in colonic flora have been observed in response to ingestion of different types of RS (LeBlay et al, 1999;Silvi et al, 1999), it is possible that ingestion of RRM for only 21 days was not sufficient to induce measurable adaptation effects.…”

Section: Discussionmentioning

confidence: 99%

Gastrointestinal responses following acute and medium term intake of retrograded resistant maltodextrins, classified as type 3 resistant starch

Storey

Lee

Bornet³

et al. 2007

Eur J Clin Nutr

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The gastrointestinal (GI) responses to ingested digestion resistant retrograded maltodextrins, having a structural similarity to type 3 resistant starch (RS) but a lower molecular weight, were studied after acute single bolus ingestion as well as during a medium-term period of daily ingestion. The overall study was split into two parts: part 1 aimed (1) to determine the GI responses of young adults following consumption of 0-60 g resistant maltodextrin; (2) to define the maximum non-effective dose (MNED) at which a considerable increase in symptoms did not occur. Part 2 aimed to determine whether a gradual increase in the daily dose of retrograded resistant maltodextrin (RRM) to a level finally exceeding by at least 10 g the individually determined MNED to acute ingestion in part 1 of the study, modified tolerance over time. Design: Study part 1 was executed as a randomized double-blind placebo-controlled crossover study and study part 2 as a longitudinal study. Subjects: Forty-one healthy adult volunteers aged 18-24 years were recruited from the student population of the University of Salford. All subjects enrolled and completed study part 1 and 39 subjects enrolled and completed study part 2. Interventions: In study part 1, individuals consumed, in random order 0, 20, 40, 60, 80, 100 or 120 g of a RRM containing starch product incorporated in pre-prepared foods on individual test days. Assuming a minimum content of 50% RRM in the starch product this delivered respectively 0, 10, 20, 30, 40, 50 or 60 g of RRM. All foods were prepared and coded by personnel not involved in carrying out the tests. Test days were separated by 7 day washout periods. In study part 2, consumption of RRM was increased from 3.6 g at day 1 in incremental doses up to each subject's MNED as determined in study 1, to be achieved at day 14. Subsequently, RRM intake was from day 15-21 in a way that the final intake at day 21 was at least 10 g above the individual MNED. In both parts of the study, subjects reported the prevalence and magnitude of GI symptoms. Results: No significant change was observed in either defecation frequency and faecal consistency or the number of subjects experiencing any GI symptoms, following consumption of foods containing 0-60 g RRM. The individual MNED at which an increase in symptoms did not occur was determined as 60 g RRM for 71% of the subjects who participated in study part 1. Regression analysis showed that consumption of gradually increasing doses of RRM in food products over 21 days was associated with a significant increase in the mean symptom score for flatulence (P ¼ 1.5 Â 10 À4 ), total bowel movement frequency (P ¼ 0.023) and bowel movement frequency to pass watery faeces (P ¼ 0.0157). Increasing the ingested dose of RRM by 10 g above the predetermined MNED, however, did not provoke significant increases in GI symptoms. In both studies, the majority of symptom responses were classified by the subjects as 'little more than usual'. Conclusions: Consumption of up to 60 g RRM is tolerated well by most i...

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“…Resistant starch selectively increased the levels of lactobacilli and bi dobacteria in faecal samples from rats associated with human micro ora. At the same time, it reduced caecal ammonia concentration, caecal pH and beta-glucuronidase activity (42).…”

Section: Prebioticsmentioning

confidence: 99%

Functional Aspects of Pro- and Prebiotics A literature review on immune modulation and influence on cancer

Mogensen

Rowland

Midtvedt

et al. 2000

Microbial Ecology in Health and Disease

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Resistant starch modifies gut microflora and microbial metabolism in human flora-associated rats inoculated with faeces from Italian and UK donors

Cited by 196 publications

References 39 publications

Suppression of azoxymethane-induced colon cancer development in rats by dietary resistant starch

Suppression of azoxymethane-induced colon cancer development in rats by dietary resistant starch

Gastrointestinal responses following acute and medium term intake of retrograded resistant maltodextrins, classified as type 3 resistant starch

Functional Aspects of Pro- and Prebiotics A literature review on immune modulation and influence on cancer

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