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 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.

BackgroundColonic fermentation of dietary-fibre to short-chain-fatty-acids (SCFA) influences appetite hormone secretion in animals, but SCFA production is excessive in obese animals. This suggests there may be resistance to the effect of SCFA on appetite-hormones in obesity.Objectivesto determine the effects of inulin (IN) and resistant-starch (RS) on postprandial SCFA, and gut hormone (GLP-1, PYY, and ghrelin) responses in healthy overweight/obese (OWO) vs lean (LN) humans.MethodsOvernight fasted participants (13 OWO, 12 LN) consumed 300mL water containing 75g glucose (GLU) as Control, or 75g glucose plus 24g IN, or 28.2g RS using a randomized, single-blind, cross-over design. Blood for appetite-hormones and SCFA was collected at intervals over 6h. A standard lunch was served 4h after the test drink.ResultsRelative to GLU, IN, but not RS, significantly increased SCFA AUC from 4–6h (AUC4-6). Neither IN nor RS affected GLP-1 or PYY-AUC4-6. Although neither IN nor RS reduced ghrelin-AUC4-6 compared to GLU, ghrelin at 6h after IN was significantly lower than that after GLU (p<0.05). After IN, relative to GLU, the changes in SCFA-AUC4-6 were negatively related to the changes in ghrelin-AUC4-6 (p=0.017). SCFA and hormone responses did not differ significantly between LN and OWO.ConclusionsAcute increases in colonic SCFA do not affect GLP-1 or PYY responses in LN or OWO subjects, but may reduce ghrelin. The results do not support the hypothesis that SCFA acutely stimulate PYY and GLP-1 secretion; however, a longer adaptation to increased colonic fermentation or a larger sample size may yield different results.