Aims: To compare the in vitro fermentation properties of pectins and oligosaccharides derived from them in pure and mixed faecal cultures. Methods and Results: Specific growth rates of selected bacterial genera were calculated in pure culture. Bifidobacterium angulatum, B. infantis and B. adolescentis had higher growth rates on pectic oligosaccharides (POS I) derived from high methylated pectin (HMP) than on HMP and B. pseudolongum and B. adolescentis on pectic oligosaccharides (POS II) derived from low methylated pectin than on HMP. Controlled pH batch mixed faecal cultures were then carried out and a prebiotic index was calculated as a mean to compare the fermentation properties of the different substrates. In general, greater fermentation selectivity was obtained with lower degrees of methylation (PI24 -HMP ¼ )0AE11, PI24 -LMP ¼ 0AE033; PI24 -POS I ¼ 0AE071 and PI 24-POS II ¼ 0AE092). An effect of size on prebiotic potential was observed, with the oligosaccharides having more selective fermentation properties than the pectins they derived from. Conclusions: The degree of methylation plays an important role in the fermentation properties of pectins. Pectic-oligosaccharides are a better prebiotic candidate than the pectins, although their bifidogenic effect is low compared to oligofructose. Significance and Impact of the Study: The effect of size on prebiotic potential was demonstrated. Non-selectively fermented polysaccharides like pectin can have their bifidogenic properties improved by partial hydrolysis.
Cardiovascular risk is determined by the complex interactions between genetic and environmental factors. The apoE genotype represents the most-widely-studied single nucleotide polymorphism in relation to CVD risk, with > 3600 publications cited in PubMed. Although originally described as a mediator of lipoprotein metabolism, the lipoprotein-independent functions of apoE are being increasingly recognised, with limited data available on the potential impact of genotype on these metabolic processes. Furthermore, although meta-analyses suggest that apoE4 carriers may have a 40-50% increased CVD risk, the associations reported in individual studies are highly heterogeneous and it is recognised that environmental factors such as smoking status and dietary fat composition influence genotype-phenotype associations. However, information is often derived from observational studies or small intervention trials in which retrospective genotyping of the cohort results in small group sizes in the rarer E2 and E4 subgroups. Either larger well-standardised intervention trials or smaller trials with prospective recruitment according to apoE genotype are needed to fully establish the impact of diet on genotype-CVD associations and to establish the potential of dietary strategies such as reduced total fat, saturated fat, or increased antioxidant intakes to counteract the increased CVD burden in apoE4 carriers. ApoE genotype: CVD: Dietary fat: Oxidative status: InflammationThe impact of single nucleotide polymorphisms on risk of chronic diseases such as CVD, and the ability of dietary factors to manipulate genotype-phenotype associations, is being increasingly recognised. Undoubtedly, the mostwidely-studied gene variant in relation to CVD is the apoE e (e2, e3, e4) genotype. Since its discovery in 1973 the central role of the apoE protein in lipoprotein metabolism has been comprehensively investigated and reported. The 40-50 % higher risk of CVD in apoE4 carriers (Song et al. 2004) has been traditionally attributed to moderately higher circulating cholesterol and TAG levels. However, it is becoming increasingly recognised that an effect on lipoprotein metabolism alone cannot explain the disease differential and that the impact of an apoE4 genotype is largely lipoprotein independent. Roles of macrophagederived apoE protein on vascular health and atherogenesis are being identified, with apoE thought to impact on oxidative status and in an autocrine and paracrine manner affect macrophage, vascular smooth muscle cell, endothelial cell and platelet function. An impact of genotype on these localised functions of apoE could in part explain the impact of genotype on CVD pathology, as will be discussed.Additionally, apoE genotype has been shown to affect the responsiveness to the total fat content and fatty acid composition of the diet. Manipulation of dietary fat content may serve as a means of reducing the increased CVD burden associated with an apoE4 genotype.
Anaerobic batch culture fermenters were used for a preliminary screening of the in vitro utilization by human gut microflora of dextran and novel oligodextrans (I, II and III) produced in the University of Reading (UK). Glucose and fructooligosaccharides (FOS) were used as reference carbohydrates. As expected, FOS acted as a good prebiotic in that it selectively increased numbers of bifidobacteria in the early stages of the fermentation. Dextran and oligodextrans each resulted in an enrichment of bifidobacteria in the batch cultures, with high levels of persistence up to 48 h. They also produced elevated levels of butyrate ranging from 5 to 14⋅85 mmol/l. To more effectively simulate conditions that prevail in different regions of the large intestine, a three-stage continuous culture cascade system was used to study further the fermentation of dextran, a low-molecular-mass oligodextran (IV) and maltodextrin. Oligodextran IV was shown to be the best substrate for bifidobacteria and lactobacilli with steady-state populations of bifidobacteria and lactobacilli being higher in all three vessels of the gut model than the respective populations resulting from dextran and maltodextrin. A maximum difference of 1⋅9 log was observed in vessel 1 for both bifidobacteria and lactobacilli in the case of dextran fermentation, while 1⋅4 log and 0⋅8 log in vessel 3 were the maximum differences for bifidobacteria and lactobacilli when maltodextrin was used as the carbohydrate source. Moreover, dextran and oligodextran appeared to stimulate butyrate production, with a maximum production up to 25⋅39 mmol/l in vessel 3 when fermenting dextran, followed by 21⋅70 mmol/l in the case of oligodextran IV and only 12⋅64 mmol/l in the case of maltodextrin.
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