Background: The consumption of plant based foods has demonstrated an inverse association with disease prevalence. Among the components of plant based foods, polyphenol and fibre are two of the main contenders for many health benefits. The majority of polyphenols and fibre pass through the small intestine unabsorbed, reaching the colon where they are subjected to the action of the colonic microbiota; resulting in the production of the potentially bioactive metabolites: phenolic acids and SCFA. These metabolites are potentially responsible for many of the health benefits exerted by polyphenols rich foods and fibre. Given the recent advances in understanding the role of colonic microbiota in metabolic and immune responses, factors, which may positively or negatively modify the composition of the colonic bacteria have also received much attention. Foods rich in dietary fibre and polyphenols have the potential to modify colonic bacteria through prebiotic and antibiotic action. The potential bacterial inhibition by polyphenolics and the stimulation of bacterial growth by fibre and polyphenols means potential for both sets of compounds to influence metabolite production from each other. Polyphenols and fibre are most often present in the same foods and may be found together in plant cell walls. Thus they most often enter the colon together. We aimed to explore how the presence of these two components in the diet may impact on the metabolite production from the other by the colonic microbiota. Methods: The food matrix interaction of fibres and polyphenols was assessed using the fibres: raftiline, pectin and ispaghula, having different physio-chemical properties (rate of fermentation and viscosity) and the polyphenols: rutin and catechin, epicatechin and other polyphenols present in cocoa in vitro models of phenolic acid and short chain fatty acid (SCFA) production. The impact of ispaghula on urinary phenolic acids after cocoa ingestion was then investigated in an acute human study. In Chapter-3 the impact of the fermentable fibres on phenolic acid production from isolated parent compound: rutin in-vitro using 24 hour batch cultures using human faecal samples from volunteers (n=10) after being on a 3-day low polyphenol diet was investigated. Using the same model the impact of rutin, quercetin and their metabolites on SCFA production from raftiline, ispaghula and pectin was then investigate. The SCFA were measured by GC-FID and phenolic acids by GCMS. pH and gas were also measured. Using the same methodology the matrix interaction between raftiline, ispaghula and pectin separately on phenolic acid production from their parent compounds within their food matrix was investigated using cocoa as a rich source of polyphenols, as well as the impact of cocoa polyphenols and their metabolites on SCFA production from the fermentable fibres (Chapter-4) In Chapter-5, 24-hour urinary polyphenolic acids were measured in 5 batches (0, 0-2, 2-5, 5-8, 8-24 hour) in 12 human volunteers after ingestion of 1g paracetamol with 20g cocoa (extra brute Cocoa-Cacao Barry, Barry Callebaut, Hardricourt, France) with water, 15g of ispaghula with water or the combination of the two. Urine samples were also used for total phenol and antioxidant capacity measurement. Plasma was collected over six hours (every half hour for 4 hours and at 6th hour) and used for the measurement of total phenols as well as paracetamol concentrations for the estimation of gastric emptying rate. Breath hydrogen was used for estimation of small bowel transit time and visual analogue scales (VAS) were used for the estimation of subjective appetite response to meals. Results: The faecal fermentation of rutin resulted in the production of the following phenolic acids: PAA, 4-HBA, 3-HPAA, 4-HPAA, 3,4-DHPAA, 3-HPPA and 4-HPPA. All of these phenolic acids were significantly reduced by at least one of the three fibres, with the exception of 3-HPPA and 4-HPPA. The extent of inhibition of total sum of phenolic acids from raftiline and pectin was similar (p < 0.01) and ispaghula demonstrated the least inhibitory effect (p=0.03). Rutin and quercetin had no impact on the SCFA production from the fermentable fibres. The phenolic acids identified from cocoa faecal incubations consisted of: of PAA, 3-HPAA, 4-HPAA, 3,4-DHPAA, 3-HPPA, 4-HPPA, 3,4-DHPPA, 4-HBA, 3,4-DHBA, hippuric acid and vanillic acid. Unlike the rutin study where majority of phenolic acids were significantly reduced, in this study only four of eleven phenolic acids were affected (PAA, 3-HPAA, 4-HPAA, 4-HBA: also inhibited in the rutin study).The extent of phenolic acid reduction was the highest for pectin (p < 0.01), followed by raftiline (p < 0.01) and ispaghula (p=0.03). These phenolic acids or their parent compounds had no impact on SCFA production from the fermentable fibres. The consumption of cocoa resulted in the urinary excretion of the following phenolic acids: 3-HPAA, 4-HPAA, 3,4-DHPAA, Hippuric, 4-HPA, 4-HBA, 3,4-DHBA, Vanillic, 4-HVA, Mandelic and 4-HMA. All of which, with the exception of vanillic acid and 3,4-DHPAA, were reduced by ispaghula (Table-I). Ispaghula accelerated gastric emptying rate but had no impact on small bowel transit time. The analysis of total phenol (TP assay) concentration (plasma and urine) and antioxidant capacity (urine) did not demonstrate any difference between cocoa and ispaghula, which were both high. However when they were ingested together there was a signification reduction in both total phenol and antioxidant capacity (p < 0.01). Given that urinary and plasma concentration of total phenols was no different for ispaghula and cocoa we analysed the free phenolic and bound phenolics in both ispaghula and cocoa, showing that cocoa has significantly higher free phenolics than ispaghula, whereas bound phenolics were higher in ispaghula. The sum of bound and free total phenols was higher in cocoa than ispaghula (approximately 10 fold). Urinary, faecal SCFA were not measured as they are not validated to represent in-vivo production. Conclusion: there is a strong inhibition of phenolic acid production from polyphenol by the fermentable fibres and their metabolites. This inhibition is stronger in-vivo than in-vitro for ispaghula, which may reflect the longer interaction time in the colon and potential small bowel interaction. The production of SCFA from fermentable fibres was not inhibited by the polyphenols or their metabolites. These interactions need to be considered when assessing the bioavailability of phenolic acid production and their potential health benefits.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:637665 |
| Date | January 2014 |
| Creators | Mansoorian, Bahareh |
| Publisher | University of Glasgow |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://theses.gla.ac.uk/6136/ |
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