['Colonic fermentation of dietary fibre produces short-chain fatty acids (SCFAs), acetate, propionate and butyrate, which may protect against type 2 diabetes by reducing serum free-fatty acids (FFAs). Since hyperinsulinaemia is associated with insulin resistance and increased diabetes risk, the main objective was to compare markers of colonic fermentation after acute inulin ingestion in subjects with normal (<40\u2009 pmol/l, NI) and high (≥40 \u2009pmol/l, HI) plasma insulin.', 'Overnight fasted NI (n=9) and HI (n=9) subjects were studied for 4 \u2009h on two separate days after consuming 300 \u2009ml drinks containing 75 \u2009g glucose (Glucose) or 75 \u2009g glucose plus 24\u2009 g inulin (Inulin) using a randomized, single-blind, crossover design.', 'Inulin elicited a higher breath hydrogen and methane areas under the curve (AUC), but the increases in SCFA responses were not statistically significant. Mean serum-acetate concentration over the 4-h study period was higher in NI than in HI subjects (44.3 ± 6.9 vs 22.5 ± 3.7 \u2009μmol/l, P=0.001). The rate of rebound of FFA was reduced by Inulin, with FFA at 4\u2009 h being less after Inulin than Glucose, regardless of insulin status (0.310 ± 0.028 vs 0.432 ± 0.042 mEq/l, P=0.008).'] Does inulin increase short-term markers for colonic fermentation similarly in healthy and hyperinsulinaemic humans?