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Scandinavian Journal of Gastroenterology 1996-Oct

Colonic production of butyrate in patients with previous colonic cancer during long-term treatment with dietary fibre (Plantago ovata seeds).

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I Nordgaard
H Hove
M R Clausen
P B Mortensen

Nøgleord

Abstrakt

BACKGROUND

Butyrate has antineoplastic properties against colorectal cancer cells and is the preferred oxidative substrate for colonocytes. Like acetate and propionate (short-chain fatty acids; SCFAs), butyrate is produced by colonic fermentation of dietary fibre.

METHODS

Twenty patients resected for colorectal cancer were treated with 20 g/day of the fibre Plantago ovata seeds for 3 months, which increased the intake of fibre by 17.9 +/- 0.8 g/day, from basal levels of 19.2 +/- 1.7 g/day; 17 patients completed the study. Faecal samples were obtained on eight occasions, twice before treatment, and monthly three times during and three time after treatment.

RESULTS

One month of fibre therapy increased faecal concentrations of butyrate by 42 +/- 12% (from 13.2 +/- 1.2 to 19.3 +/- 3.0 mmol/l; P < 10(-4)), acetate by 25 +/- 6% (P < 10(-4)), propionate by 28 +/- 9% (P = 0.01), and total SCFAs by 25 +/- 6% (P < 10 (-4)). Concentrations were increased during the 3-month fibre treatment but reversed to pretreatment levels within 1 to 2 months after cessation of fibre supplementation. The relative concentration (ratio) of butyrate was not altered owing to a simultaneous increase in acetate and propionate. Faecal pH decreased initially but was normalized after 2 months of fibre supplements. Fibre therapy increased the 24-h productions of butyrate by 47 +/- 10% (P < 10(-4)) and acetate by 50 +/- 7% (P < 10(-4)) in 16.6% faecal homogenates with added P. ovata seeds (20mg/ml), but SCFA productions returned to pretreatment levels after discontinuation of additional fibre intakes.

CONCLUSIONS

Oral intake of P. ovata seeds adapted the colonic flora to increase the production of butyrate (and acetate) from this fibre and increased faecal concentrations of butyrate by 42% in patients resected for colonic cancer. The effects depended on continuity of treatment.

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