Background/Objectives:High dietary fibre intakes may protect against obesity by influencing colonic fermentation and the colonic microbiota. Though, recent studies suggest that increased colonic fermentation contributes to adiposity. Diet influences the composition of the gut microbiota. Previous research has not evaluated dietary intakes, body mass index (BMI), faecal microbiota and short chain fatty acid (SCFA) in the same cohort. Our objectives were to compare dietary intakes, faecal SCFA concentrations and gut microbial profiles in healthy lean (LN, BMI⩽25) and overweight or obese (OWOB, BMI>25) participants.Design:We collected demographic information, 3-day diet records, physical activity questionnaires and breath and faecal samples from 94 participants of whom 52 were LN and 42 OWOB.Results:Dietary intakes and physical activity levels did not differ significantly between groups. OWOB participants had higher faecal acetate (P=0.05), propionate (P=0.03), butyrate (P=0.05), valerate (P=0.03) and total short chain fatty acid (SCFA; P=0.02) concentrations than LN. No significant differences in Firmicutes to Bacteroides/Prevotella (F:B) ratio was observed between groups. However, in the entire cohort, Bacteroides/Prevotella counts were negatively correlated with faecal total SCFA (r=−0.32, P=0.002) and F:B ratio was positively correlated with faecal total SCFA (r=0.42, P<0.0001). Principal component analysis identified distinct gut microbiota and SCFA–F:B ratio components, which together accounted for 59% of the variation. F:B ratio loaded with the SCFA and not with the microbiota suggesting that SCFA and F:B ratio vary together and may be interrelated.Conclusions:The results support the hypothesis that colonic fermentation patterns may be altered, leading to different faecal SCFA concentrations in OWOB compared with LN humans. More in-depth studies looking at the metabolic fate of SCFA produced in LN and OWOB participants are needed in order to determine the role of SCFA in obesity.

BackgroundShort-chain fatty acids (SCFA) are produced by colonic microbiota from dietary carbohydrates and proteins that reach the colon. It has been suggested that SCFA may promote obesity via increased colonic energy availability. Recent studies suggest obese humans have higher faecal SCFA than lean, but it is unclear if this difference is due to increased SCFA production or reduced absorption.ObjectivesTo compare rectal SCFA absorption, dietary intake and faecal microbial profile in lean (LN) versus overweight and obese (OWO) individuals.DesignEleven (11) LN and 11 OWO individuals completed a 3-day diet record, provided a fresh faecal sample and had SCFA absorption measured using the rectal dialysis bag method. The procedures were repeated after two weeks.ResultsAge-adjusted faecal SCFA concentration was significantly higher in OWO than LN (81.3 ± 7.4 vs. 64.1 ± 10.4 mmol/kg, P = 0.023). SCFA absorption (24.4 ± 0.8 vs 24.7 ± 1.2%, respectively, P =0.787) and dietary intakes were similar between the groups, except for a higher fat intake in OWO. However, fat intake did not correlate with SCFAs or bacterial abundance. OWO had higher relative Firmicutes abundance (83.1 ± 4.1 vs 69.5 ± 5.8%, respectively, P = 0.008) and a higher Firmicutes:Bacteriodetes ratio (P = 0.023) than LN. There was a positive correlation between Firmicutes and faecal SCFA within the whole group (r =0.507, P =0.044), with a stronger correlation after adjusting for available carbohydrate (r = 0.615, P =0.005).ConclusionsThe higher faecal SCFA in OWO subjects is not due to differences in SCFA absorption or diet. Our results are consistent with the hypothesis that OWO subjects produce more colonic SCFA than LN due to differences in colonic microbiota. However, further studies are needed to prove this.

Background/ObjectivesColonic fermentation of dietary fibre produces short-chain fatty-acids (SCFA) acetate, propionate and butyrate, which may protect against type 2 diabetes by reducing serum free-fatty acids (FFA). Since hyperinsulinemia 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 (< 40pmol/L, NI) and high (≥ 40pmol/L, HI) plasma-insulin.Subjects/MethodsOvernight fasted NI (n = 9) and HI (n = 9) subjects were studied for 4 h on 2 separate days after consuming 300 ml drinks containing 75 g glucose (Glucose) or 75 g glucose plus 24 g inulin (Inulin) using a randomized, single-blind, cross-over design.ResultsInulin elicited a higher breath hydrogen and methane AUC but the increases in SCFA responses were not statistically significant. Overall mean serum-acetate over the 4 h study period was higher in NI than HI subjects (44.3±6.9 vs 22.5±3.7 μmol/L, p = 0.001). The rate of rebound of FFA was reduced by Inulin, with FFA at 4hr being less after Inulin than Glucose, regardless of insulin status (0.310±0.028 vs 0.432±0.042 mEq/L, p = 0.008).ConclusionsThis suggests that inulin increases short-term markers for colonic fermentation but a longer study period may be necessary to observe differences in SCFA production. The reason for the lower serum-acetate in HI is unclear but may be due to reduced absorption, increased clearance or decreased endogenous production. This suggests the need to compare acetate kinetics in normal and hyperinsulinemic subjects.

Background/ObjectivesColonic-fermentation of dietary-fibre to short-chain fatty-acids (SCFA) may protect against obesity and diabetes, but excess production of colonic SCFA has been implicated in the promotion of obesity. We aimed to compare the effects of two fermentable-fibres on postprandial SCFA and second-meal glycaemic response in healthy overweight or obese (OWO) vs lean (LN) participants.Methodsusing a randomized cross-over design, 13 OWO and 12 LN overnight fasted participants were studied for 6h on 3 separate days after consuming 300mL water containing 75g glucose(GLU) as control or with 24g inulin(IN) or 28g resistant-starch(RS). A standard lunch was served 4h after the test-drink.ResultsWithin the entire group, compared to control, IN significantly increased serum SCFA (p<0.001) but had no effect on FFA or second-meal glucose and insulin responses. In contrast, RS had no significant effect on SCFA but reduced FFA rebound (p<0.001) and second-meal glucose (p=0.002) and insulin responses (p=0.024). OWO had similar postprandial serum SCFA and glucose concentrations but significantly greater insulin and FFA than LN. However, the effects of IN and RS on SCFA, glucose, insulin and FFA responses were similar in LN and OWO.ConclusionsResistant-starch has favorable second-meal effects, likely related to changes in FFA rather than SCFA concentrations. However, a longer study may be needed to demonstrate an effect of RS on SCFA. We found no evidence that acute increases in SCFA after IN reduce glycaemic responses in humans, and we were unable to detect a significant difference in SCFA responses between OWO vs LN subjects.

Recent attention has focused on the significance of colonic Archaea in human health and energy metabolism. The main objectives of this study were to determine the associations among the number of fecal Archaea, body mass index (BMI), fecal short chain fatty acid (SCFA) concentrations, and dietary intakes of healthy humans. We collected demographic information, 3-d diet records, and breath and fecal samples from 95 healthy participants who were divided into 2 groups: detectable Archaea (>10(6) copies/g; Arch+ve) and undetectable Archaea. Dietary intakes, BMI, and fecal SCFAs were similar in both groups. The mean number of Archaea 16S rRNA gene copies detected in Arch+ve participants' feces was 8.9 ± 0.2 log/g wet weight. In Arch+ve participants, there were positive correlations between breath methane and age (r = 0.52; P = 0.001), total dietary fiber (TDF) intake (r = 0.57; P = 0.0003), and log number of fecal Archaea 16S rRNA gene copies (r = 0.35; P = 0.03). In the Arch+ve group, negative correlations were observed between TDF/1000 kcal and fecal total SCFA (r = -0.46; P ≤ 0.01) and between breath methane and fecal total SCFA (r = -0.42; P = 0.01). Principal component analysis identified a distinct Archaea factor with positive loadings of age, breath methane, TDF, TDF/1000 kcal, and number of log Archaea 16S rRNA gene copies. The results suggest that colonic Archaea is not associated with obesity in healthy humans. The presence of Archaea in humans may influence colonic fermentation by altering SCFA metabolism and fecal SCFA profile.