International Journal of Molecular Sciences,
Год журнала:
2019,
Номер
20(9), С. 2134 - 2134
Опубликована: Апрель 30, 2019
Autism
spectrum
disorders
(ASD)
are
a
group
of
neurodevelopmental
characterized
by
deficits
in
social
interaction
and
communication,
repetitive
behaviors.
In
addition,
co-morbidities
such
as
gastro-intestinal
problems
have
frequently
been
reported.
Mutations
deletion
proteins
the
SH3
multiple
ankyrin
repeat
domains
(SHANK)
gene-family
were
identified
patients
with
ASD,
Shank
knock-out
mouse
models
display
autism-like
phenotypes.
SHANK3
not
only
expressed
central
nervous
system
(CNS).
Here,
we
show
expression
gastrointestinal
(GI)
epithelium
report
significantly
different
GI
morphology
Shank3
(KO)
mice.
Further,
detected
altered
microbiota
composition
measured
feces
KO
mice
that
may
contribute
to
inflammatory
responses
affecting
brain
development.
line
this,
found
higher
E.
coli
lipopolysaccharide
levels
liver
samples
mice,
an
increase
Interleukin-6
activated
astrocytes
We
conclude
apart
from
its
well-known
role
CNS,
plays
specific
tract
ASD
phenotype
extracerebral
mechanisms.
Objective
Non-alcoholic
fatty
liver
disease
(NAFLD)-associated
hepatocellular
carcinoma
(HCC)
is
an
increasing
healthcare
burden
worldwide.
We
examined
the
role
of
dietary
cholesterol
in
driving
NAFLD–HCC
through
modulating
gut
microbiota
and
its
metabolites.
Design
High-fat/high-cholesterol
(HFHC),
high-fat/low-cholesterol
or
normal
chow
diet
was
fed
to
C57BL/6
male
littermates
for
14
months.
Cholesterol-lowering
drug
atorvastatin
administered
HFHC-fed
mice.
Germ-free
mice
were
transplanted
with
stools
from
different
diets
determine
direct
modulated-microbiota
NAFLD–HCC.
Gut
analysed
by
16S
rRNA
sequencing
serum
metabolites
liquid
chromatography–mass
spectrometry
(LC–MS)
metabolomic
analysis.
Faecal
microbial
compositions
59
hypercholesterolemia
patients
39
healthy
controls.
Results
High
led
sequential
progression
steatosis,
steatohepatitis,
fibrosis
eventually
HCC
mice,
concomitant
insulin
resistance.
Cholesterol-induced
formation
associated
dysbiosis.
The
composition
clustered
distinctly
along
stages
steatohepatitis
HCC.
Mucispirillum,
Desulfovibrio,
Anaerotruncus
Desulfovibrionaceae
increased
sequentially;
while
Bifidobacterium
Bacteroides
depleted
which
corroborated
human
hypercholesteremia
patients.
Dietary
induced
bacterial
alteration
including
taurocholic
acid
decreased
3-indolepropionic
acid.
gavaged
HFHC
manifested
hepatic
lipid
accumulation,
inflammation
cell
proliferation.
Moreover,
restored
cholesterol-induced
dysbiosis
completely
prevented
development.
Conclusions
drives
inducing
Cholesterol
inhibitory
therapy
manipulation
may
be
effective
strategies
prevention.
Nutrients,
Год журнала:
2020,
Номер
12(10), С. 3197 - 3197
Опубликована: Окт. 20, 2020
A
high-fat
diet
(HFD)
can
easily
induce
obesity
and
change
the
gut
microbiota
its
metabolites.
However,
studies
on
effects
of
diets
host
have
drawn
inconsistent
results.
In
this
study,
unexpected
results
showed
that
refined
HFD
increased
diversity
short-chain
fatty
acids
(SCFAs),
causing
an
increase
in
energy
metabolism.
Further
analysis
revealed
these
changes
were
caused
by
different
fiber
content
two
diets.
Male
C57BL/6J
mice
(4–5
weeks
old)
fed
either
or
low-fat
(LFD)
for
14
weeks.
The
metabolic
rates,
thermogenesis,
microbiome,
intestinal
SCFAs
tested.
triggered
disturbed
glucose
homeostasis.
Mice
ingested
more
than
LFD
(p
<
0.0001),
higher
SCFA
concentrations
related
to
abundances
specific
bacteria
group.
Also,
heat
up-regulated
thermogenesis
genes
uncoupling
protein
1(Ucp-1),
peroxisome
proliferator-activated
receptor-γ
coactivator-1α
(Pgc-1α)
expression
brown
adipose
tissue
(BAT).
It
was
16S
rRNA
gene
sequencing
microbial
diversity,
which
enriched
Desulfovibrionaceae,
Rikenellaceae
RC9
group,
Mucispirillum,
meanwhile,
reduced
abundance
Lactobacillus,
Bifidobacterium,
Akkermansia,
Faecalibaculum,
Blautia.
predicted
pathways
indicated
non-absorbed
carbohydrate
metabolism
pathways,
as
well
risks
colonization
pathogens
inflammation.
conclusion,
obesogenic
male
mice,
intake
from
drove
SCFAs,
expenditure.
Meanwhile,
differences
nutrient
dissociate
broad
expenditure,
microbiota,
metabolites
obesity,
raising
doubts
previous
studies.
Therefore,
it
is
necessary
consider
whether
will
interfere
with
experiments.
Betaine
is
a
natural
compound
present
in
commonly
consumed
foods
and
may
have
potential
role
the
regulation
of
glucose
lipids
metabolism.
However,
underlying
molecular
mechanism
its
action
remains
largely
unknown.
Here,
we
show
that
supplementation
with
betaine
contributes
to
improved
high-fat
diet
(HFD)-induced
gut
microbiota
dysbiosis
increases
anti-obesity
strains
such
as
Food Science and Human Wellness,
Год журнала:
2022,
Номер
11(3), С. 502 - 511
Опубликована: Фев. 4, 2022
Polyphenols,
including
phenolic
acids,
flavonoids,
and
procyanidins,
are
abundant
in
food
beverage
derived
from
plants.
Tea
(Camellia
sinensis)
is
particularly
rich
polyphenols
(e.g.,
catechins,
theaflavins,
thearubigins,
gallic
acid,
flavonols),
which
thought
to
contribute
the
health
benefits
of
tea.
High
intake
tea
has
been
described
prevent
and/or
attenuate
a
variety
chronic
pathological
conditions
like
cardiovascular
diseases,
neurodegenerative
diabetes,
cancer.
This
review
focuses
on
established
antioxidant
anti-inflammatory
properties
underlying
mechanisms
their
involvement
inflammatory
bowel
diseases
(IBD).
act
as
efficient
antioxidants
by
inducing
an
endogenous
defense
system
maintaining
intracellular
redox
homeostasis.
also
regulate
signaling
pathways
such
nuclear
factor-κB,
activator
protein
1,
signal
transducer
transcriptions,
factor
E2-related
2,
associated
with
IBD
development.
Accumulating
pieces
evidence
have
indicated
that
enhance
epithelial
barrier
function
improve
gut
microbial
dysbiosis,
contributing
management
colitis.
Therefore,
this
study
suggests
supplementation
could
outcome
patients
IBD.
Nature Microbiology,
Год журнала:
2023,
Номер
8(10), С. 1863 - 1879
Опубликована: Сен. 11, 2023
Abstract
Alterations
in
the
gut
microbiome,
including
diet-driven
changes,
are
linked
to
rising
prevalence
of
food
allergy.
However,
little
is
known
about
how
specific
bacteria
trigger
breakdown
oral
tolerance.
Here
we
show
that
depriving
specific-pathogen-free
mice
dietary
fibre
leads
a
microbiota
signature
with
increases
mucin-degrading
bacterium
Akkermansia
muciniphila
.
This
associated
intestinal
barrier
dysfunction,
increased
expression
type
1
and
2
cytokines
IgE-coated
commensals
colon,
which
result
an
exacerbated
allergic
reaction
allergens,
ovalbumin
peanut.
To
demonstrate
causal
role
A.
,
employed
tractable
synthetic
human
gnotobiotic
mice.
The
presence
within
microbiota,
combined
deprivation,
resulted
stronger
anti-commensal
IgE
coating
innate
type-2
immune
responses,
worsened
symptoms
Our
study
provides
important
insights
into
microbes
can
regulate
pathways
allergy
diet-dependent
manner.