Metabolic
syndrome
(MetS)
is
intricately
linked
to
dysregulation
of
gut
microbiota
and
host
metabolomes.
Here,
we
first
find
that
a
purified
citrus
polymethoxyflavone-rich
extract
(PMFE)
potently
ameliorates
high-fat
diet
(HFD)-induced
MetS,
alleviates
dysbiosis,
regulates
branched-chain
amino
acid
(BCAA)
metabolism
using
16S
rDNA
amplicon
sequencing
metabolomic
profiling.
The
metabolic
protective
effects
PMFE
are
dependent,
as
demonstrated
by
antibiotic
treatment
fecal
microbiome
transplantation
(FMT).
modulation
altered
BCAA
levels
in
the
serum
feces,
which
were
significantly
associated
with
features
actively
responsive
therapeutic
interventions
PMFE.
Notably,
greatly
enriched
commensal
bacterium
Bacteroides
ovatus,
gavage
B.
ovatus
reduced
concentrations
alleviated
MetS
HFD
mice.
may
be
used
prebiotic
agent
attenuate
target-specific
microbial
species
have
unique
promise
for
diseases.
The
human
gut
harbors
more
than
100
trillion
microbial
cells,
which
have
an
essential
role
in
metabolic
regulation
via
their
symbiotic
interactions
with
the
host.
Altered
ecosystems
been
associated
increased
and
immune
disorders
animals
humans.
Molecular
linking
microbiota
host
energy
metabolism,
lipid
accumulation,
immunity
also
identified.
However,
exact
mechanisms
that
link
specific
variations
composition
of
development
obesity
diseases
humans
remain
obscure
owing
to
complex
etiology
these
pathologies.
In
this
review,
we
discuss
current
knowledge
about
mechanistic
between
microbiota,
system
context
disease,
a
focus
on
importance
axis
links
microbes
inflammation.
Finally,
therapeutic
approaches
aimed
at
reshaping
ecosystem
regulate
related
pathologies,
as
well
challenges
area.
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.
Journal of Clinical Investigation,
Год журнала:
2019,
Номер
129(10), С. 4050 - 4057
Опубликована: Сен. 30, 2019
The
metabolic
syndrome
(MetS)
is
a
constellation
of
risk
factors
that,
if
left
untreated,
will
often
progress
to
greater
defects
such
as
type
2
diabetes
and
nonalcoholic
fatty
liver
disease.
While
these
have
been
established
for
over
40
years,
the
definition
MetS
warrants
reconsideration
in
light
substantial
data
that
emerged
from
studies
gut
microbiome.
In
this
Review
we
present
existing
recent
literature
supports
microbiome's
potential
influence
on
various
MetS.
interplay
intestinal
microbiota
with
host
metabolism
has
shown
be
mediated
by
myriad
factors,
including
defective
barrier,
bile
acid
metabolism,
antibiotic
use,
pleiotropic
effects
microbially
produced
metabolites.
These
show
events
start
gut,
response
external
cues
diet
circadian
disruption,
far-reaching
beyond
gut.
