Abstract
Humans are living in an increasingly 'obesogenic' environment with easily accessed, energy dense foods and sedentary lifestyles, which is resulting in a gradual increase in the population body weight. The need for strategies to prevent the rise in obesity are therefore becoming increasingly urgent. One strategy is to identify and develop foods that enhance satiety. The recently discovered short-chain fatty acid (SCFA) activated G-coupled protein receptors GPR41 and GPR43 are co-localised in L-cells with the anorexigenic gut hormone PYY, and also in adipocytes, with activation stimulating leptin release. Thus SCFA such as acetate and propionate may enhance satiety. The findings from a series of randomised controlled crossover studies investigating orally (Chapters 3-5) and colonically (Chapter 7) delivered SCFA effects on appetite and metabolic response are reported herein. Appetite was assessed subjectively with a battery of visual analogues scales (VAS), and quantitatively with an ad libitum buffet meal 3-h (Chapters 3-5) or 7-h (Chapter 7) postprandially and using 24-h diet diaries. The role of propionate was investigated in the first study (Chapter 3). Participants (n=20) consumed breakfast made with propionate-rich sourdough (SOUR, 6.0 mmol propionate), or equally palatable, isocaloric placebo (PL, 0.1 mmol propionate) bread. SOUR did not influence subjective nor quantitative appetite measures and appeared to increase postprandial insulinaemia relative to PL (p=0.061, treatment x time). By contrast, ingestion of 25 mmol acetate (within vinegar) in an unpalatable (Unpal) or more palatable (Pal) drink alongside a standard breakfast (n=16), significantly increased rated fullness (p<0.0001) and nausea (p=0.001), decreased rated prospective consumption (p=0.036) and hunger (p=0.045) and reduced 24-h EI (p=0.021) and postprandial glycaemia (p=0.022) relative to PL (no acetate). Appetite measures were significantly correlated to breakfast palatability ratings (p<0.05), and Unpal significantly reduced EI relative to PL (p<0.05), while Pal did not. In a follow-up study to further examine the role of palatability (Chapter 5), orosensory stimulation with a vinegar-containing drink (VIN) following a standard preload did not significantly alter postprandial metabolites nor alter EI 3 h postprandially. However VAS hunger ratings were significantly lower (p=0.009, treatment x time) relative to PL, suggesting a transient reduction in appetite following orosensory stimulation with VIN. Colonic SCFA effects were investigated by providing 22.4g inulin, 25.5g L-rhamnose (L-Rha) or no NDC (PL) in split doses at breakfast and lunch alongside standard mixed meals (n=13) following a 6-d run-in (Chapter 7). NDC treatment did not influence quantitative nor subjective appetite measures, except desire to eat a meal (p=0.008, during morning). However, postprandial plasma insulin (p=0.009) and NEFA (p=0.046, following lunch) were significantly influenced (treatment x time effect), with the lowest response for both following L-Rha, previously reported to enhance serum propionate. Additionally the ability of a novel non-digestible carbohydrate (inulin esterified with propionate) to enhance colonic propionate production was investigated (Chapter 6), although the results were inconclusive. The findings from these investigations are mixed, but overall do not support a role for SCFA in appetite regulation and are suggestive that previously reported effects may arise, at least in part, from product palatability. L-Rha shows promise as a candidate to reduce postprandial insulin secretion.