Colonic fermentation of inulin increases whole-body acetate turnover in dogs.

Metabolism of acetate from colonic fermentation was investigated in dogs. Beagle dogs (n = 9) were fed a control diet for 17 d followed by a 3% inulin-enriched diet (from chicory) for 4 and 21 d. On 3 occasions, the dogs were administered simultaneously infusions of [1-(13)C]acetate i.v. and [1,2-(13)C(2)]acetate intrarectally. Peripheral acetate concentration and turnover did not change over time after consumption of an inulin-enriched diet for 4 d. After 21 d of consuming the inulin-enriched diet, the whole-body acetate turnover increased significantly by 31% from (mean +/- SEM) 15.6 +/- 2.2 to 20.4 +/- 2.9 micromol/(kg . min) without a change in concentration. The rate of colonic acetate production that reached the peripheral circulation was 4.8 +/- 1.8 micromol/(kg . min). However, no [1,2-(13)C(2)]acetate tracer was recovered in the peripheral circulation. The fraction of oxidized tracer was higher in the gut (64 +/- 3%) than in peripheral circulation (46 +/- 3%) in dogs fed an inulin-enriched diet for 21 d. In conclusion, colonic fermentation of inulin occurred and indirectly stimulated whole-body acetate turnover in dogs fed an inulin-enriched diet for 21 d.