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Increases in snack consumption associated with Westernized lifestyles provide an opportunity to introduce nutritious foods into poor diets. We describe two 10-wk-long open label, single group assignment human studies that measured the effects of two snack prototypes containing fiber preparations from two sustainable and scalable sources; the byproducts remaining after isolation of protein from the endosperm of peas and the vesicular pulp remaining after processing oranges for the manufacture of juices. The normal diets of study participants were supplemented with either a pea- or orange fiber-containing snack. We focused our analysis on quantifying the abundances of genes encoding carbohydrate-active enzymes (CAZymes) (glycoside hydrolases and polysaccharide lyases) in the fecal microbiome, mass spectrometric measurements of glycan structures (glycosidic linkages) in feces, plus aptamer-based assessment of levels of 1,300 plasma proteins reflecting a broad range of physiological functions. Computational methods for feature selection identified treatment-discriminatory changes in CAZyme genes that correlated with alterations in levels of fiber-associated glycosidic linkages; these changes in turn correlated with levels of plasma proteins representing diverse biological functions, including transforming growth factor type β/bone morphogenetic protein-mediated fibrosis, vascular endothelial growth factor-related angiogenesis, P38/MAPK-associated immune cell signaling, and obesity-associated hormonal regulators. The approach used represents a way to connect changes in consumer microbiomes produced by specific fiber types with host responses in the context of varying background diets.

Changing food preferences brought about by westernization that have deleterious health effects1,2-combined with myriad forces that are contributing to increased food insecurity-are catalysing efforts to identify more nutritious and affordable foods3. Consumption of dietary fibre can help to prevent cardiovascular disease, type 2 diabetes and obesity4-6. A substantial number of reports have explored the effects of dietary fibre on the gut microbial community7-9. However, the microbiome is complex, dynamic and exhibits considerable intra- and interpersonal variation in its composition and functions. The large number of potential interactions between the components of the microbiome makes it challenging to define the mechanisms by which food ingredients affect community properties. Here we address the question of how foods containing different fibre preparations can be designed to alter functions associated with specific components of the microbiome. Because a marked increase in snack consumption is associated with westernization, we formulated snack prototypes using plant fibres from different sustainable sources that targeted distinct features of the gut microbiomes of individuals with obesity when transplanted into gnotobiotic mice. We used these snacks to supplement controlled diets that were consumed by adult individuals with obesity or who were overweight. Fibre-specific changes in their microbiomes were linked to changes in their plasma proteomes indicative of an altered physiological state.

Purpose: The aim of this pilot study was to analyze concomitantly the kinetics of production of 13C-labeled gut-derived metabolites from 13C-labeled wheat bran in three biological matrices (breath, plasma, stools), in order to assess differential fermentation profiles among subjects. Methods: Six healthy women consumed a controlled breakfast containing 13C-labeled wheat bran biscuits. H2, CH4 and 13CO2, 13CH4 24 h-concentrations in breath were measured, respectively, by gas chromatography (GC) and GC-isotope ratio mass spectrometry (GC-IRMS). Plasma and fecal concentrations of 13C-short-chain fatty acids (linear SCFAs: acetate, propionate, butyrate, valerate; branched SCFAs: isobutyrate, isovalerate) were quantified using GC-combustion-IRMS. Gut microbiota composition was assessed by16S rRNA gene sequencing analysis. Results: H2 and CH4 24 h-kinetics distinguished two groups in terms of fermentation-related gas excretion: high-CH4 producers vs low-CH4 producers (fasting concentrations: 45.3 ± 13.6 ppm vs 6.5 ± 3.6 ppm). Expired 13CH4 was enhanced and prolonged in high-CH4 producers compared to low-CH4 producers. The proportion of plasma and stool 13C-butyrate tended to be higher in low-CH4 producers, and inversely for 13C-acetate. Plasma branched SCFAs revealed different kinetics of apparition compared to linear SCFAs. Conclusion: This pilot study allowed to consider novel procedures for the development of biomarkers revealing dietary fiber-gut microbiota interactions. The non-invasive assessment of exhaled gas following 13C-labeled fibers ingestion enabled to decipher distinct fermentation profiles: high-CH4 producers vs low-CH4 producers. The isotope labeling permits a specific in vivo characterisation of the dietary fiber impact consumption on microbiota metabolite production. Clinical trial registration: The study has been registered under the number NCT03717311 at ClinicalTrials.gov on October 24, 2018. [ABSTRACT FROM AUTHOR]

Dietary cholesterol oxidation products (COPs) were reported to exhibit in vitro toxicity toward vascular cells. The aim of this study was to determine whether dietary COPs induce in vivo toxicity toward coronary arteries and to evaluate their effect on the coronary reactivity. Golden Syrian hamsters were fed either a normolipidic diet or a hyperlipidic diet with or without a mixture of COPs (1.4 mg/kg/day). At the end of the feeding periods, cardiac mitochondria and cytosol were prepared to determine the subcellular distribution of cytochrome c. Oxidative phosphorylation was evaluated with glutamate, pyruvate or palmitoylcarnitine as a substrate. The main coronary artery was examined all along its length by transmission electron microscopy (TEM). Plasma sterol concentrations were determined. Furthermore, at the end of the 3–month feeding period, the hearts were perfused at constant pressure by the Langendorff method. The endothelium–dependent reactivity to acetylcholine was evaluated. The myocardial sterol concentration was also estimated. After a 15–day diet with dietary COPs, a release of cytochrome c into the cytosolic fraction of the whole heart occurred, which indicated apoptosis of one or several types of cardiac cells probably induced by excess circulating cholestanetriol. The morphological data obtained by TEM after three months of diet suggested that mainly vascular cells (endothelial and smooth muscle cells) were damaged by dietary COPs, whereas cardiomyocytes appeared healthy. Furthermore, the mitochondrial oxidation of palmitoylcarnitine was reduced and that of pyruvate was increased, suggesting some maintenance of energy metabolism. This strengthens the hypothesis of apoptosis. Several changes in coronary reactivity suggesting an increased NO production were observed. In conclusion, dietary COPs triggered in vivo apoptosis of coronary cells through the release of cytochrome c in the cytosol. This toxicity was counterbalanced by an increased endothelium–dependent dilation. [ABSTRACT FROM AUTHOR]

An official method for determining food glycemic index (GI) was published by the Organization for International Standardization (ISO) in 2010, but its performance has not been assessed. Therefore, we aimed to determine the intra- and inter-laboratory variation of food GI values measured using the 2010 ISO method. Three laboratories (Australia, Canada and France) determined the GI and insulinemic-index (II) of six foods in groups of 13–15 participants using the 2010 ISO method and intra- and inter-laboratory Standard Deviations (SDs) were calculated. Overall mean food GIs varied from 47 to 86 (p < 0.0001) with no significant difference among labs (p = 0.57) and no food × laboratory interaction (p = 0.20). Within-laboratory SD was similar among foods (range, 17.8–22.5; p = 0.49) but varied among laboratories (range 17.5–23.1; p = 0.047). Between-laboratory SD of mean food GI values ranged from 1.6 to 6.7 (mean, 5.1). Mean glucose and insulin responses varied among foods (p < 0.001) with insulin (p = 0.0037), but not glucose (p = 0.054), varying significantly among labs. Mean II varied among foods (p < 0.001) but not among labs (p = 0.94). In conclusion, we found that using the 2010 ISO method, the mean between-laboratory SD of GI was 5.1. This suggests that the ISO method is sufficiently precise to distinguish a mean GI = 55 from a mean GI ≥ 70 with 97–99% probability. [ABSTRACT FROM AUTHOR]