In vitro fecal fermentation is an assay that uses fecal microbes
to ferment foods, the results of which can be used to
evaluate the potential of prebiotic candidates. To date, there
have been various protocols used for in vitro fecal fermentation-
based assessments of food substances. In this study,
we investigated how personal gut microbiota differences and
external factors affect the results of in vitro fecal fermentation
assays. We used Cheonggukjang (CGJ), a Korean traditional
fermented soybean soup that is acknowledged as
healthy functional diet. CGJ was digested in vitro using acids
and enzymes, and then fermented with human feces anaerobically.
After fecal fermentation, the microbiota was analyzed
using MiSeq, and the amount of short chain fatty acids
(SCFAs) were measured using GC-MS. Our results suggest
that CGJ was effectively metabolized by fecal bacteria to produce
SCFAs, and this process resulted in an increase in the
abundance of Coprococcus, Ruminococcus, and Bifidobacterium
and a reduction in the growth of Sutterella, an opportunistic
pathogen. The metabolic activities predicted from the
microbiota shifts indicated enhanced metabolism linked to
methionine biosynthesis and depleted chondroitin sulfate
degradation. Moreover, the amount of SCFAs and microbiota
shifts varied depending on personal microbiota differences.
Our findings also suggest that in vitro fecal fermentation of
CGJ for longer durations may partially affect certain fecal
microbes. Overall, the study discusses the usability of in vitro
gastrointestinal digestion and fecal fermentation (GIDFF)
to imitate the effects of diet-induced microbiome modulation
and its impact on the host.
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The DNA damage checkpoint signaling pathway is a highly
conserved surveillance mechanism that ensures genome integrity
by sequential activation of protein kinase cascades.
In mammals, the main pathway is orchestrated by two central
sensor kinases, ATM and ATR, that are activated in response
to DNA damage and DNA replication stress. Patients
lacking functional ATM or ATR suffer from ataxia-telangiectasia
(A-T) or Seckel syndrome, respectively, with pleiotropic
degenerative phenotypes. In addition to DNA strand
breaks, ATM and ATR also respond to oxidative DNA damage
and reactive oxygen species (ROS), suggesting an unconventional
function as regulators of intracellular redox status.
Here, we summarize the multiple roles of ATM and ATR, and
of their orthologs in Saccharomyces cerevisiae, Tel1 and Mec1,
in DNA damage checkpoint signaling and the oxidative stress
response, and discuss emerging ideas regarding the possible
mechanisms underlying the elaborate crosstalk between those
pathways. This review may provide new insights into the integrated
cellular strategies responsible for maintaining genome
stability in eukaryotes with a focus on the yeast model
organism.
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