Frontiers in Nutrition,
Journal Year:
2025,
Volume and Issue:
12
Published: March 24, 2025
Chronic
liver
disease
is
defined
by
persistent
harm
to
the
that
might
result
in
decreased
function.
The
two
prevalent
chronic
diseases
are
alcohol-associated
(ALD)
and
metabolic
dysfunction-associated
steatotic
(MASLD).
There
ample
evidence
pathogenesis
of
these
closely
linked
gastrointestinal
dysfunctions
alters
gut-liver
crosstalk.
These
alterations
mediated
through
imbalances
gut
microbiota
composition/function
combined
with
disruption
barrier
integrity
allows
for
harmful
microbes
their
toxins
enter
portal
circulation
reach
elicit
an
inflammatory
response.
This
leads
further
recruitment
systemic
cells,
such
as
neutrophils,
T-cells,
monocytes
into
liver,
which
perpetuate
additional
inflammation
development
progressive
damage.
Many
therapeutic
modalities,
currently
used
prevent,
attenuate,
or
treat
aimed
at
modulating
dysbiosis
improving
intestinal
Betaine
a
choline-derived
metabolite
methyl
group
donor
antioxidant,
anti-inflammatory
osmoprotectant
properties.
Studies
have
shown
low
betaine
levels
associated
higher
organ
been
several
publications
demonstrating
role
supplementation
preventing
ALD
MASLD.
review
explores
protective
effects
its
capacity
regulate
maintain
prevent
diseases.
Further
studies
needed
enhance
our
understanding
potential
could
pave
way
targeted
interventions
management
not
only
diseases,
but
other
bowel
conditions.
Gut Microbes,
Journal Year:
2023,
Volume and Issue:
15(1)
Published: July 28, 2023
Gut
microbiota-diet
interaction
has
been
identified
as
a
key
factor
of
metabolic
associated
fatty
liver
disease
(MAFLD).
Recent
studies
suggested
that
dietary
polyphenols
may
protect
against
MAFLD
by
regulating
gut
microbiota;
however,
the
underlying
mechanisms
remain
elusive.
We
first
investigated
effects
cyanidin
3-glucoside
and
its
phenolic
metabolites
on
high-fat
diet
induced
in
C57BL/6J
mice,
protocatechuic
acid
(PCA)
showed
significant
positive
effect.
Next,
regulation
PCA
lipid
metabolism
microbiota
were
explored
mouse
model
fecal
transplantation
(FMT)
experiment.
Dietary
reduced
intraperitoneal
hepatic
fat
deposition
with
lower
levels
transaminases
(AST
&
ALT)
inflammatory
cytokines
(IL-1β,
IL-2,
IL-6,
TNF-α
MCP-1),
but
higher
HDL-c/LDL-c
ratio.
Characterization
indicated
decreased
Firmicutes/Bacteroidetes
ratio
mainly
reducing
relative
abundance
genus
Enterococcus,
which
was
positively
correlated
LDL-c,
AST,
ALT
most
up-regulated
lipids
lipidomics
analysis.
FMT
experiments
Enterococcus
faecalis
caused
inflammation,
insulin
resistance
expression
carnitine
palmitoyltransferase-1
alpha
(CPT1α),
can
be
reversed
through
inhibiting
faecalis.
Transcriptomics
analysis
decrease
fibroblast
growth
1
(Fgf1),
recovered
Fgf1
insulin-like
binding
protein
2
(Igfbp2),
receptor
substrate
(Irs1)
(Irs2).
These
results
demonstrated
high
proportion
accelerates
CPT1α
Fgf1,
prevented
supplementation
PCA.
The
laxative
lubiprostone
has
been
shown
to
decrease
intestinal
permeability.
We
aimed
assess
the
safety
and
efficacy
of
administered
for
48
weeks
in
patients
with
metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD).
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(22), P. 16502 - 16502
Published: Nov. 19, 2023
Cirrhosis
is
the
end
result
of
liver
fibrosis
in
chronic
diseases.
Studying
mechanisms
its
development
and
developing
measures
to
slow
down
regress
it
based
on
this
knowledge
seem
be
important
tasks
for
medicine.
Currently,
disorders
gut–liver
axis
have
great
importance
pathogenesis
cirrhosis.
However,
gut
dysbiosis,
which
manifests
as
increased
proportions
microbiota
Bacilli
Proteobacteria
that
are
capable
bacterial
translocation
a
decreased
proportion
Clostridia
strengthen
intestinal
barrier,
occurs
even
at
pre-cirrhotic
stage
disease.
This
leads
translocation,
process
by
those
microbes
enter
blood
portal
vein
then
tissue,
where
they
activate
Kupffer
cells
through
Toll-like
receptor
4.
In
response,
produce
profibrogenic
cytokines,
hepatic
stellate
cells,
stimulating
their
transformation
into
myofibroblasts
collagen
other
elements
extracellular
matrix.
Blocking
with
antibiotics,
probiotics,
synbiotics,
methods
could
progression
fibrosis.
was
shown
number
animal
models
but
requires
further
verification
long-term
randomized
controlled
trials
humans.
Nutrients,
Journal Year:
2023,
Volume and Issue:
15(18), P. 3970 - 3970
Published: Sept. 14, 2023
Metabolism-associated
fatty
liver
disease
(MAFLD)
is
a
multifaceted
that
involves
complex
interactions
between
various
organs,
including
the
gut
and
heart.
It
defined
by
hepatic
lipid
accumulation
related
to
metabolic
dysfunction,
obesity,
diabetes.
Understanding
intricate
interplay
of
gut–liver–heart
crosstalk
crucial
for
unraveling
complexities
MAFLD
developing
effective
treatment
prevention
strategies.
The
gut–liver
participates
in
regulation
inflammatory
processes
through
host–microbiome
interactions.
Gut
microbiota
have
been
associated
with
development
progression
MAFLD,
its
dysbiosis
contributes
insulin
resistance,
inflammation,
oxidative
stress.
Metabolites
derived
from
enter
systemic
circulation
influence
both
heart,
resulting
axis
playing
an
important
role
MAFLD.
Furthermore,
growing
evidence
suggests
endothelial
inflammation
may
contribute
increased
risk
cardiovascular
(CVD).
Additionally,
dysregulation
metabolism
also
lead
cardiac
dysfunction
heart
failure.
Overall,
molecular
pathways
CVD
patients
This
review
emphasizes
current
understanding
as
foundation
optimizing
patient
outcomes
Heliyon,
Journal Year:
2024,
Volume and Issue:
10(9), P. e30387 - e30387
Published: April 25, 2024
Non-alcoholic
fatty
liver
disease
(NAFLD)
has
become
one
of
the
most
frequent
chronic
diseases
worldwide
in
recent
decades.
Metabolic
like
excessive
blood
glucose,
central
obesity,
dyslipidemia,
hypertension,
and
function
abnormalities
cause
NAFLD.
NAFLD
significantly
increases
likelihood
cancer,
heart
disease,
mortality,
making
it
a
leading
transplants.
steatohepatitis
(NASH)
is
more
advanced
form
that
causes
scarring
inflammation
over
time
can
ultimately
result
cirrhosis
hepatocellular
carcinoma.
In
this
review,
we
briefly
discuss
NAFLD's
pathogenic
mechanisms,
their
progression
into
NASH
afterward
to
NASH-related
cirrhosis.
It
also
covers
epidemiology,
metabolic
glucose
lipid
metabolism
liver,
macrophage
dysfunction,
bile
acid
toxicity,
stellate
cell
stimulation.
Additionally,
consider
contribution
intestinal
microbiota,
genetics,
epigenetics,
ecological
factors
fibrosis
carcinoma
risk
patients.
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(12), P. 1800 - 1800
Published: June 7, 2024
Gut
microbiota
might
affect
the
severity
and
progression
of
metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD).
We
aimed
to
characterize
gut
dysbiosis
clinical
parameters
regarding
fibrosis
stages
assessed
by
magnetic
resonance
elastography.
This
study
included
156
patients
with
MASLD,
stratified
into
no/mild
(F0–F1)
moderate/severe
(F2–F4).
Fecal
specimens
were
sequenced
targeting
V4
region
16S
rRNA
gene
analyzed
using
bioinformatics.
The
genotyping
PNPLA3,
TM6SF2,
HSD17B13
was
allelic
discrimination
assays.
Our
data
showed
that
microbial
profiles
between
groups
significantly
differed
in
beta-diversity
but
not
alpha-diversity
indices.
Enriched
Fusobacterium
Escherichia_Shigella,
depleted
Lachnospira
found
F2–F4
group
versus
F0–F1
group.
Compared
F0–F1,
had
elevated
plasma
surrogate
markers
epithelial
permeability
bacterial
translocation.
genera,
PNPLA3
polymorphisms,
old
age,
diabetes
independently
associated
advanced
multivariable
analyses.
Using
Random
Forest
classifier,
signature
three
genera
could
differentiate
high
diagnostic
accuracy
(AUC
0.93).
These
results
indicated
imbalance
enriched
pathogenic
decreased
beneficial
bacteria,
association
several
genetic
factors,
potential
contributors
pathogenesis
MASLD.