Fibre alimentaire

Résumé

Les fibres alimentaires sont les parties d'un aliment d'origine végétale constituées de mélanges complexes de glucides provenant de la paroi cellulaire (polyosides pariétaux tels que les celluloses, les hémicelluloses, les pectines, les lignines) ou du cytoplasme des cellules végétales (polyosides cytoplasmiques, glucides de réserve tels que des gommes et des mucilages), et qui ne peuvent pas être complètement décomposées par les enzymes digestives humaines. Par extension, ce terme désigne les fibres végétales dont la dégradation chez les animaux herbivores ou omnivores implique le microbiote intestinal, écosystème digestif microbien vivant en symbiose avec son hôte et qui est le seul à posséder un vaste répertoire d'enzymes agissant en synergie pour hydrolyser ces fibres. Les fibres sont indispensables au bon fonctionnement du transit intestinal et à la santé globale des humains, car métabolisées par le microbiote intestinal en produits qui influencent l'ensemble de leurs métabolis

Source officielle

https://fr.wikipedia.org/wiki/Fibre_alimentaire

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Computational Approaches for Studying Dietary Behaviors with Digital Traces

Kristina Gligoric

Human nutrition and dietary habits shape our health, daily life, societies, the environment, and life on earth in general. However, it remains challenging to understand and attempt to change dietary behaviors using traditional methods due to measurement and causal identification challenges.In this thesis, we contribute computational and causal approaches leveraging large-scale passively sensed digital traces to shed new light on our dietary behaviors and derive novel scientific insights. We study dietary behaviors in two types of contexts: campus-wide and worldwide. Based on digital traces capturing behaviors of tens of thousands of people on campus and millions of internet users, we develop observational study designs that enable the isolation of causal effects of implicit behavioral interventions, including forming social ties, being exposed to the food choice of others, and stay-at-home interventions. The thesis is organized into three parts.The first part presents studies based on situated on-campus food purchase logs. In the first study, we show how, when a person acquires a new eating partner on campus, the healthiness of their food choice shifts significantly in the direction of their new eating partner's dietary patterns. In the second study, we identify purchasing mimicry, i.e., copying the food choices of others in the purchasing queue, as a specific behavioral mechanism for how similarities in dietary behaviors between individuals occur on campus. The second part of the thesis leverages online information-seeking traces (Google search query logs). Studying worldwide dietary behaviors, we identify and describe global shifts in dietary interests during the first wave of the COVID-19 pandemic, larger and longer-lasting than the typical changes during the end-of-year holidays in Western countries.In the third part, we critically investigate the limits to how much computational approaches can reveal about dietary behaviors in the general population. We contribute a framework for reasoning about biases of digital traces and present a case study of food consumption in Switzerland. The bias estimates derived in the case study imply that researchers should aim to establish evidence of validity before relying on social media and tracking apps---two frequently used digital traces---as proxies for true food consumption in the general population.The novel scientific findings and methodological advances presented here contribute to the existing knowledge about human dietary behaviors and inform the design of future food systems, policies, and behavioral interventions.

EPFL2022

Chargement

The progressive decline of muscle mass and function called sarcopenia is a multi-factorial process associated to frailty, disability, and low quality of life in the elderly. The co-factor nicotinamide adenine dinucleotide (NAD+) becomes a limiting factor in the course of aging and other pathological conditions. It has emerged as a major regulator of cellular metabolism, which is modulated by dietary precursors of the vitamin B3 family. So far, no direct link between sarcopenia and alterations in NAD+ metabolism has been reported. In this thesis, I have taken a multi-disciplinary approach combining molecular profiling in humans and dietary and genetic manipulations in rodents to characterize the skeletal muscle NAD+ metabolism in the context of muscle plasticity and aging. We have performed a multi-center study to characterize the molecular signature of human sarcopenia compared to age-matched controls. Sarcopenic participants of three cohorts in Singapore, the United Kingdom and Jamaica presented a prominent transcriptional signature of mitochondrial dysfunction, which translated into functional bioenergetic deficiency with lower mitochondrial protein expression and activity. Furthermore, we established a concurrent decrease in NAD+ content of sarcopenic muscle, which correlated to lower muscle strength and function in these patients. Supplementation with the dietary NAD+ precursor nicotinamide riboside (NR) was shown to improve pathological muscle conditions and revert age-related mitochondrial dysfunction and stem cell senescence in mice. To test whether boosting NAD+ through NR can be beneficial in the context of sarcopenia, we investigated the acute response to NR supplementation in young adult and old sarcopenic rats. Acute NR treatment efficiently increased NAD+ levels and normalized specific age-related gene expression signatures in old rats, in particular related to fibrosis. Interestingly, our transcriptional profiling also revealed that the molecular response to NR is partially blunted in aging and suggests that aged muscle could be in a state of partial NAD+ resistance. To investigate the role of endogenous NR as NAD+ precursor in the muscle, we studied mice deficient for NR kinases 1 and 2 (NRK1/2 dKO), the rate-limiting enzymes for NR salvage. NRK1/2 dKO mice develop normally, but exhibit elevated salvage of the NAD+ precursor nicotinamide (NAM) to maintain tissue NAD+. Thus, our results demonstrate for the first time that an endogenous NRK-dependent flux actively converts NR into NAD+ in healthy skeletal muscle. Moreover, we demonstrated that NRKs are required for muscle regeneration, as dKO mice failed to efficiently regenerate the NAD+ pool during the active phases of myofiber remodeling, which coincided with a transient delay of myofiber maturation. Conversely, dietary NR improved the activation of muscle stem cells and accelerated recovery of NAD+ levels in regenerating myofibers of wild-type mice. Altogether, this work demonstrates that both in humans and preclinical models, sarcopenia is tightly linked to mitochondrial bioenergetics and NAD+ metabolism. Dietary manipulation of NAD+ levels is a promising therapeutic strategy for the management of age-related muscle dysfunction for which we uncovered important mechanistic insights linking metabolic fluxes through the NAD+ pathway to physiological adaptations.

EPFL2019

Chargement

Gut microbial transformation of the dietary mutagen MeIQx may reduce exposure levels without altering intestinal transport

Julita Maria Stadnicka-Michalak, Jianbo Zhang

The mutagen and probable human carcinogen 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) is metabolized in the colon to 9-hydroxyl-2,7-dimethyl-7,9,10,11-tetrahydropyrimido[2',1':2,3]imidazo[4,5-f]quinoxaline (MeIQx-M1) by conjugation with microbially generated acrolein. However, whether this microbiota-controlled process alters systemic exposure and hepatotoxicity of MeIQx remains unclear. The physiological relevance of this microbial transformation on the systemic exposure of MeIQx was investigated using an in vitro-in vivo extrapolation approach. To address whether microbial transformation influences intestinal transport of MeIQx, the intestinal uptake of MeIQx and its metabolite MeIQx-M1 was quantified using Ussing chambers mounted with different intestinal segments from male Fischer 344 rats. Up to 0.4% of both MeIQx and MeIQx-M1 were transported from the mucosa] side to the serosal side of intestinal tissue within 90 min, suggesting that the intestinal uptake of both compounds is similar. With the uptake rates of both compounds, physiologically based pharmacokinetic (PBPK) modeling of the fate of MeIQx in the human body including microbial transformation of MeIQx was performed. Results indicate for the first time that high levels of microbe-derived acrolein would be required to significantly reduce systemic exposure of MeIQx in humans. Finally, neither MeIQx nor MeIQx-M1 were cytotoxic towards human liver HepaRG cells at dietary or higher concentrations of MeIQx. In summary, these findings suggest that gut microbial transformation of heterocyclic amines has the potential to influence systemic human exposure to some extent, but may require significant gut microbial production of acrolein and that further investigations are needed to understand physiological levels of acrolein and competing biotransformation pathways.

PERGAMON-ELSEVIER SCIENCE LTD2019

Chargement

EPFL2019

Computational Approaches for Studying Dietary Behaviors with Digital Traces

Kristina Gligoric

EPFL2022

Gut microbial transformation of the dietary mutagen MeIQx may reduce exposure levels without altering intestinal transport

Julita Maria Stadnicka-Michalak, Jianbo Zhang

PERGAMON-ELSEVIER SCIENCE LTD2019