A novel gastrointestinal microbiome modulator from soy pods reduces absorption of dietary fat in mice

Boué, Stephen M.; Fortgang, Ilana S.; Levy, Ronald J; Bhatnagar, Deepak; Burow, Matthew E.; Fahey, G. C.; Heiman, Mark L.

doi:10.1002/oby.21197

Cited by 20 publications

(20 citation statements)

References 36 publications

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“…This practice could also handicap the plant's own defense system by eliminating the need for the plant to produce phytoalexins [18] . Phytoalexins may provide key micronutrients that expand the GI microbiome when ingested [19] . Thus, economic pressures force agricultural practices that have limited the richness of the GI microbiome over the past century.…”

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confidence: 99%

A healthy gastrointestinal microbiome is dependent on dietary diversity

Heiman¹,

Greenway

2016

Molecular Metabolism

276

193

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BackgroundLike all healthy ecosystems, richness of microbiota species characterizes the GI microbiome in healthy individuals. Conversely, a loss in species diversity is a common finding in several disease states. This biome is flooded with energy in the form of undigested and partially digested foods, and in some cases drugs and dietary supplements. Each microbiotic species in the biome transforms that energy into new molecules, which may signal messages to physiological systems of the host.Scope of reviewDietary choices select substrates for species, providing a competitive advantage over other GI microbiota. The more diverse the diet, the more diverse the microbiome and the more adaptable it will be to perturbations. Unfortunately, dietary diversity has been lost during the past 50 years and dietary choices that exclude food products from animals or plants will narrow the GI microbiome further.Major conclusionAdditional research into expanding gut microbial richness by dietary diversity is likely to expand concepts in healthy nutrition, stimulate discovery of new diagnostics, and open up novel therapeutic possibilities.

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confidence: 99%

A healthy gastrointestinal microbiome is dependent on dietary diversity

Heiman¹,

Greenway

2016

Molecular Metabolism

276

193

View full text Add to dashboard Cite

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“…Additionally, patulin has been shown to decompose at pHs above 6 [49]. As feces of mice typically show a pH of 7.4 (e.g., [50]), we cannot exclude that patulin was already destabilized and could not exert a highly inhibiting function in this physiological condition. The local influence of intact patulin molecules on single microbial niches in the gut cannot be fully excluded, as only representative genera derived from feces were investigated in this study.…”

Section: Discussionmentioning

confidence: 99%

Identification of Patulin from Penicillium coprobium as a Toxin for Enteric Neurons

et al. 2019

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The identification and characterization of fungal commensals of the human gut (the mycobiota) is ongoing, and the effects of their various secondary metabolites on the health and disease of the host is a matter of current research. While the neurons of the central nervous system might be affected indirectly by compounds from gut microorganisms, the largest peripheral neuronal network (the enteric nervous system) is located within the gut and is exposed directly to such metabolites. We analyzed 320 fungal extracts and their effect on the viability of a human neuronal cell line (SH-SY5Y), as well as their effects on the viability and functionality of the most effective compound on primary enteric neurons of murine origin. An extract from P. coprobium was identified to decrease viability with an EC50 of 0.23 ng/µL in SH-SY5Y cells and an EC50 of 1 ng/µL in enteric neurons. Further spectral analysis revealed that the effective compound was patulin, and that this polyketide lactone is not only capable of evoking ROS production in SH-SY5Y cells, but also diverse functional disabilities in primary enteric neurons such as altered calcium signaling. As patulin can be found as a common contaminant on fruit and vegetables and causes intestinal injury, deciphering its specific impact on enteric neurons might help in the elaboration of preventive strategies.

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“…The dried fecal samples were minced and extracted with 75% ethanol (5 mg/1 mL) at 50 °C for 2 h. The extract was centrifuged and 100 μL of supernatant was diluted with 500 μL PBS for assay. The TBA was analyzed enzymatically using the assay kit (EFBA‐100, BioAssay Systems) according to the manufacturer's instructions (Boué et al., ).…”

Section: Methodsmentioning

confidence: 99%