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Duncan, G. J.

Publications and source records attributed to Duncan, G. J..

2 recordsLinked to original sources

Simulated digestion, uptake and colonic fermentation of Gorse (Ulex europeaus) suggests safe use as a source of protein concentrates and potential bioactives.

BackgroundInvasive plants such as Gorse (Ulex europeaus) may serve as a potentially sustainable source of edible proteins and bioactives through the production of leaf protein concentrates (GLPC). The digestion, uptake and safety of phytochemicals from GLPC and the protein depleted but bioactive rich fraction (PDF) from Gorse was studied using an in vitro simulated digestion model. ResultsBoth the Gorse fractions and their digesta maintained the viability of cultured (Caco-2) intestinal cells above the 80% threshold, suggesting a lack of overt toxicity. In the digestion model, most of the plant metabolites in the digesta were largely confined to the apical fraction of the Caco-2 monolayer (representing the lumen) and were subsequently expected to be delivered to the colon. Food matrix had a significant but marginal effect on the permeability of metabolites across the Caco-2 monolayer. Lastly, in vitro intestinal microbial action appeared to produce beneficial compounds such as enterolactones, and equol. ConclusionThe Gorse fractions lack general overt toxicity to Caco-2 cells. GLPC and PDF provide metabolic substrates for the colonic microbes to produce secondary compounds that are associated with positive health outcomes.

biochemistry↗

Remyelination protects neurons from DLK-mediated neurodegeneration

Chronic demyelination and oligodendrocyte loss deprive neurons of crucial support. It is the degeneration of neurons and their connections that drives progressive disability in demyelinating disease. However, whether chronic demyelination triggers neurodegeneration and how it may do so remain unclear. We characterize two genetic mouse models of inducible demyelination, one distinguished by effective remyelination and the other by remyelination failure and chronic demyelination. While both demyelinating lines feature axonal damage, mice with blocked remyelination have elevated neuronal apoptosis and altered microglial inflammation, whereas mice with efficient remyelination do not feature neuronal apoptosis and have improved functional recovery. Remyelination incapable mice show increased activation of kinases downstream of dual leucine zipper kinase (DLK) and phosphorylation of c-Jun in neuronal nuclei. Pharmacological inhibition or genetic disruption of DLK block c-Jun phosphorylation and the apoptosis of demyelinated neurons. Together, we demonstrate that remyelination is associated with neuroprotection and identify DLK inhibition as protective strategy for chronically demyelinated neurons. HighlightsO_LICharacterization of a transgenic mouse model of demyelination without subsequent remyelination C_LIO_LIRemyelination protects neurons from axon loss and neuronal apoptosis C_LIO_LIMAPK and c-Jun phosphorylation are increased in mice featuring remyelination failure C_LIO_LIDLK is necessary for the apoptosis of chronically demyelinated neurons C_LI

neuroscience↗