Mastication effects on carotenoid bioaccessibility from mango fruit tissue

The release of carotenoids from fresh fruits or vegetables is determined by the encapsulating plant tissue matrix, intracellular carotenoid location within the cell, and the mastication process. The objectives of this study were to assess the particle sizes obtained after mastication of mango fruit tissue, and how the resulting degree of plant tissue rupture affects carotenoid bioaccessibility. A fine and a coarse chewer were selected after screening 20 healthy volunteers for in vivo human mastication, and the collected chewed boluses were subjected to wet sieving fractionation, followed by an in vitro gastric and small intestinal digestion model. Confocal micrographs show that the smallest particle size fraction (0.075 mm) consists mostly of fragmented cells and the largest size fraction (2.8 mm) contains bulky clusters of whole cells and vascular fibers. Higher amounts of total carotenoids (211–320 μg/100 g) were observed in the larger particle size fraction (2.8 mm) relative to the 1 mm (192–249 μg/100 g) and 0.075 mm fractions (136–199 μg/100 g). Smaller particles showed a greater % release of total carotenoids after in vitro digestion. Xanthophyll derivatives are more bioaccessible than β-carotene for all particle sizes. The effects of particle size or degree of fine vs coarse chewing are unexpectedly small (p > 0.05), but the process of chewing substantially reduced the release of β-carotene and xanthophylls by 34% and 18%, respectively. While there is a (small) particle size effect, this appears to not be the primary factor controlling bioaccessibility for soft tissues such as mango, in contrast to previous reports that a single cell wall appears to be enough to prevent bioaccessibility of carotenoids in more robust carrot tissues

Nutrients

The gut microbiome is involved in nutrient metabolism and produces metabolites that, via the gut-brain axis, signal to the brain and influence cognition. Human studies have so far had limited success in identifying early metabolic alterations linked to cognitive aging, likely due to limitations in metabolite coverage or follow-ups. Older persons from the Three-City population-based cohort who had not been diagnosed with dementia at the time of blood sampling were included, and repeated measures of cognition over 12 subsequent years were collected. Using a targeted metabolomics platform, we identified 72 circulating gut-derived metabolites in a case-control study on cognitive decline, nested within the cohort (discovery n = 418; validation n = 420). Higher serum levels of propionic acid, a short-chain fatty acid, were associated with increased odds of cognitive decline (OR for 1 SD = 1.40 (95% CI 1.11, 1.75) for discovery and 1.26 (1.02, 1.55) for validation). Additional analyses suggested mediation by hypercholesterolemia and diabetes. Propionic acid strongly correlated with blood glucose (r = 0.79) and with intakes of meat and cheese (r > 0.15), but not fiber (r = 0.04), suggesting a minor role of prebiotic foods per se, but a possible link to processed foods, in which propionic acid is a common preservative. The adverse impact of propionic acid on metabolism and cognition deserves further investigation.COGINUT : Cognition, anti-oxydants, acides gras: approche interdisciplinaire du rôle de la nutrition dans le vieillissement du cerveauHistoire naturelle du déclin cognitif et du besoin de soins chez le sujet âg

The serum metabolome mediates the concert of diet, exercise, and neurogenesis, determining the risk for cognitive decline and dementia

INTRODUCTION: Diet and exercise influence the risk of cognitive decline (CD) and dementia through the food metabolome and exercise-triggered endogenous factors, which use the blood as a vehicle to communicate with the brain. These factors might act in concert with hippocampal neurogenesis (HN) to shape CD and dementia. METHODS: Using an in vitro neurogenesis assay, we examined the effects of serum samples from a longitudinal cohort (n = 418) on proxy HN readouts and their association with future CD and dementia across a 12-year period. RESULTS: Altered apoptosis and reduced hippocampal progenitor cell integrity were associated with exercise and diet and predicted subsequent CD and dementia. The effects of exercise and diet on CD specifically were mediated by apoptosis. DISCUSSION: Diet and exercise might influence neurogenesis long before the onset of CD and dementia. Alterations in HN could signify the start of the pathological process and potentially represent biomarkers for CD and dementia.Identification of dietary modulators of cognitive ageing and brain plasticity and proof of concept of efficacy for preventing-reversing cognitive declin

Microbial biotransformation of polyphenols during in vitro colonic fermentation of masticated mango and banana

Mango and banana cell structures, which survived in vivo mastication and in vitro gastrointestinal digestion, were fermented in vitro for 48 h. For both fruits, flavonoids and phenolic acids were liberated and underwent microbial metabolism involving ring fission, dehydroxylation and decarboxylation. UHPLC-PDA/Q-ToF-MS profiles revealed rapid degradation (72-78%) of most intact precursors (epicatechin and several unidentified compounds) within 10 h, before the exponential phase of the cumulative gas production. Concomitant formation of catabolites (e.g. 4-hydroxyphenylacetic acid) occurred within 4-8 h, while metabolism of catechin derivative and 3-(4-hydroxyphenyl)propanoic acid continued slowly for at least 48 h, suggesting intact plant cell walls can be a controlling factor in microbial susceptibility. Untargeted PCA and OPLS-DA demonstrated clear classifications in the compositional fruit type and compound profiles as a function of time. Clusters and distinct discriminating compounds were recognised, which could lead to subsequent biomarker identification for establishing differences in polyphenol microbial metabolism of various fruit matrices

In vitro fermentation of chewed mango and banana: particle size, starch and vascular fibre effects

Fruits (and vegetables) contain cellular structures that are not degraded by human digestive enzymes. Therefore, the structure of the insoluble fraction of swallowed fruits is mostly retained until intestinal microbial fermentation. In vitro fermentation of mango and banana cell structures, which survived in vivo mastication and in vitro gastrointestinal digestion, were incubated with porcine faecal inoculum and showed intensive metabolic activity. This included degradation of cell walls, leading to the release of encapsulated cell contents for further microbial metabolism. Production of cumulative gas, short chain fatty acids and ammonia were greater for mango than for banana. Microscopic and spectroscopic analyses showed this was due to a major fermentation-resistant starch fraction present in banana, that was absent in mango. This study demonstrated distinctive differences in the fermentability of banana and mango, reflecting a preferential degradation of (parenchyma) fleshy cell walls over resistant starch in banana, and the thick cellulosic vascular fibres in mango

Cereal dietary fibres influence retention time of digesta solid and liquid phases along the gastrointestinal tract

Nutrient digestion kinetics are determined by gastric emptying (GE) in the stomach and apparent mean retention time (aMRT) along the small and large intestine. This study aimed to evaluate the effects of cereal dietary fibres (DF), either as intrinsic components of plant foods or added ingredients, on the retention of solid and liquid phases of digesta along the gastrointestinal (GI) tract. Thirty pigs were fed one of five diets containing whole wheat (WW), wheat starch (WS) or wheat starch partially replaced by wheat arabinoxylan (AX) or oat β-glucan (βG), or in combination (WSAXβG). Indigestible solid and liquid phase markers were added to each diet and fed at i) constant and ii) pulse dose intervals. Constant markers (acid insoluble ash and chromium) provided aMRT along 11 sections of the GI tract, while pulse dose markers (cerium, ytterbium and cobalt), fed 2–6 h before anaesthesia, provided a GE time. aMRT was slowest in the caecum and large intestine (LI, 15.4h), followed by the small intestine (SI, 3.4h) and stomach (2.6h) with liquid phases moving faster compared to solid phases. Between DF, AX but not βG, delayed GE of solid and liquid contents and showed longer retention time in SI and LI. In the absence of isolated soluble fibres, WS and WW diets showed similar flow characteristics of solid and liquid phases. The aMRT was shown to be dependent on the structure and swellability of added DF.</p

Food and Microbiota Metabolites Associate with Cognitive Decline in Older Subjects:A 12-Year Prospective Study

International audienceScope Diet is considered an important modulator of cognitive decline and dementia, but the available evidence is, however, still fragmented and often inconsistent. Methods and Results The article studies the long-term prospective Three-City Cohort, which consists of two separate nested case-control sample sets from different geographic regions (Bordeaux, n = 418; Dijon, n = 424). Cognitive decline is evaluated through five neuropsychological tests (Mini-Mental State Examination, Benton Visual Retention Test, Isaac's Set Test, Trail-Making Test part A, and Trail-Making Test part B). The food-related and microbiota-derived circulating metabolome is studied in participants free of dementia at baseline, by subjecting serum samples to large-scale quantitative metabolomics analysis. A protective association is found between metabolites derived from cocoa, coffee, mushrooms, red wine, the microbial metabolism of polyphenol-rich foods, and cognitive decline, as well as a negative association with metabolites related to unhealthy dietary components, such as artificial sweeteners and alcohol. Conclusion These results provide insight into the early metabolic events that are associated with the later risk to develop cognitive decline within the crosstalk between diet, gut microbiota and the endogenous metabolism, which can help identify potential targets for preventive and therapeutic strategies to preserve cognitive health

Apolipoprotein E and sex modulate fatty acid metabolism in a prospective observational study of cognitive decline

International audienceBACKGROUND: Fatty acids play prominent roles in brain function as they participate in structural, metabolic and signaling processes. The homeostasis of fatty acids and related pathways is known to be impaired in cognitive decline and dementia, but the relationship between these metabolic disturbances and common risk factors, namely the ɛ4 allele of the apolipoprotein E (ApoE-ɛ4) gene and sex, remains elusive. METHODS: In order to investigate early alterations associated with cognitive decline in the fatty acid-related serum metabolome, we here applied targeted metabolomics analysis on a nested case-control study (N=368), part of a prospective population cohort on dementia.RESULTS: When considering the entire study population, circulating levels of free fatty acids, acyl-carnitines and pantothenic acid were found to be increased among those participants who had greater odds of cognitive decline over a 12-year follow-up. Interestingly, stratified analyses indicated that these metabolomic alterations were specific for ApoE-ɛ4 non-carriers and women.CONCLUSIONS: Altogether, our results highlight that the regulation of fatty acids and related metabolic pathways during ageing and cognitive decline depends on complex inter-relationships between the ApoE-ε4 genotype and sex. A better understanding of the ApoE-ɛ4 and sex dependent modulation of metabolism is essential to elucidate the individual variability in the onset of cognitive decline, which would help develop personalized therapeutic approaches

Exploration of the Gut–Brain Axis through Metabolomics Identifies Serum Propionic Acid Associated with Higher Cognitive Decline in Older Persons

The gut microbiome is involved in nutrient metabolism and produces metabolites that, via the gut–brain axis, signal to the brain and influence cognition. Human studies have so far had limited success in identifying early metabolic alterations linked to cognitive aging, likely due to limitations in metabolite coverage or follow-ups. Older persons from the Three-City population-based cohort who had not been diagnosed with dementia at the time of blood sampling were included, and repeated measures of cognition over 12 subsequent years were collected. Using a targeted metabolomics platform, we identified 72 circulating gut-derived metabolites in a case–control study on cognitive decline, nested within the cohort (discovery n = 418; validation n = 420). Higher serum levels of propionic acid, a short-chain fatty acid, were associated with increased odds of cognitive decline (OR for 1 SD = 1.40 (95% CI 1.11, 1.75) for discovery and 1.26 (1.02, 1.55) for validation). Additional analyses suggested mediation by hypercholesterolemia and diabetes. Propionic acid strongly correlated with blood glucose (r = 0.79) and with intakes of meat and cheese (r > 0.15), but not fiber (r = 0.04), suggesting a minor role of prebiotic foods per se, but a possible link to processed foods, in which propionic acid is a common preservative. The adverse impact of propionic acid on metabolism and cognition deserves further investigation