Machine learning models for predicting metabolic dysfunction-associated steatotic liver disease prevalence using basic demographic and clinical characteristics
Journal of Translational Medicine,
Год журнала:
2025,
Номер
23(1)
Опубликована: Март 28, 2025
Metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD)
is
a
global
health
concern
that
necessitates
early
screening
and
timely
intervention
to
improve
prognosis.
The
current
diagnostic
protocols
for
MASLD
involve
complex
procedures
in
specialised
medical
centres.
This
study
aimed
explore
the
feasibility
of
utilising
machine
learning
models
accurately
screen
large
populations
based
on
combination
essential
demographic
clinical
characteristics.
A
total
10,007
outpatients
who
underwent
transient
elastography
at
First
Affiliated
Hospital
Gannan
Medical
University
were
enrolled
form
derivation
cohort.
Using
eight
characteristics
(age,
educational
level,
height,
weight,
waist
hip
circumference,
history
hypertension
diabetes),
we
built
predictive
(classified
as
none
or
mild:
controlled
attenuation
parameter
(CAP)
≤
269
dB/m;
moderate:
269-296
severe:
CAP
>
296
dB/m)
employing
10
algorithms:
logistic
regression
(LR),
multilayer
perceptron
(MLP),
extreme
gradient
boosting
(XGBoost),
bootstrap
aggregating,
decision
tree,
K-nearest
neighbours,
light
machine,
naive
Bayes,
random
forest,
support
vector
machine.
These
externally
validated
using
National
Health
Nutrition
Examination
Survey
(NHANES)
2017-2023
datasets.
In
hospital
outpatient
cohort,
algorithms
demonstrated
robust
capabilities.
Notably,
LR
achieved
highest
accuracy
(ACC)
0.711
test
cohort
0.728
validation
coupled
with
areas
under
receiver
operating
characteristic
curve
(AUC)
values
0.798
0.806,
respectively.
Similarly,
MLP
XGBoost
showed
promising
results,
achieving
an
ACC
0.735
registering
AUC
0.798.
External
NHANES
datasets
yielded
consistent
(0.831),
(0.823),
(0.784)
performing
robustly.
constructed
can
general
population.
approach
significantly
enhances
feasibility,
accessibility,
compliance
provides
effective
tool
large-scale
assessments
strategies.
Язык: Английский
Schematic Assessment of Metabolic Signatures of Non-alcoholic Fatty Liver Disease by Bridging Endocrinology and Internal Medicine: A Precision Therapy-Based Meta-Analysis
Cureus,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 28, 2025
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
seen
as
a
health
concern
globally
and
identified
via
complex
interactions
of
metabolic
dysfunctions.
Metabolomic
lipidomic
profiling
has
been
emerged
promising
tool
for
non-invasive
diagnosis
precision
therapy.
This
systematic
review
meta-analysis
aimed
to
assess
the
affect
signatures
associated
with
NAFLD
progression
their
utility
in
paving
path
medicine.
A
comprehensive
literature
search
was
conducted
adherence
guidelines
Preferred
Reporting
Items
Systematic
Reviews
Meta-Analyses
(PRISMA)
2020.
Appropriate
data
studies
were
pooled
check
using
random
effects
model.
Risk
bias
certainty
evidence
assessed
Cochrane
risk
tool,
ROBINS-I
("Risk
Of
Bias
In
Non-randomized
Studies
-
Interventions"),
Grading
Recommendations,
Assessment,
Development
Evaluation
(GRADE)
framework
respectively.
found
distinct
metabolite
patterns
especially
amino
acids,
lipids,
gut-derived
metabolites
that
correlated
severity
NAFLD.
The
findings
revealed
hazard
ratio
0.98
(95%
CI:
0.83-1.15)
indicated
no
significant
association
between
assessment
link
progression.
High
heterogeneity
observed
(I²
=
82%).
generally
low
moderate,
but
overall
rated
moderate
due
inconsistency
imprecision.
Metabolic
offered
valuable
insights
discoveries
into
pathophysiology
stratification.
However,
high
across
limited
current
clinical
applicability.
Standardized
methodologies
longitudinal
validation
needed
combine
care.
Язык: Английский
Polychlorinated Biphenyl Exposure Alters tRNA Transcriptome in High-Fat Diet-Fed Mouse Liver
Non-Coding RNA,
Год журнала:
2025,
Номер
11(3), С. 41 - 41
Опубликована: Май 22, 2025
Background/Objectives:
Exposure
of
high-fat
diet
(HFD)-fed
mice
to
polychlorinated
biphenyls
(PCBs)
results
in
metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD)
and
progression
steatohepatitis
(MASH).
The
mechanisms
by
which
HFD
PCBs
increase
MASLD
are
unclear.
Previously,
we
identified
differences
HFD-fed
mouse
tRNA
modifications
with
single
oral
exposures
the
dioxin-like
PCB126,
non-dioxin-like
PCB
mixture
Aroclor
1260
(Ar1260),
or
combination
Ar1260
+
PCB126.
Methods:
Here,
used
small
RNA
sequencing
analysis
expression
(tRAX)
pipeline
examine
if
alter
transcriptome,
including
tRNA-derived
fragments
(tRFs),
livers
PCB-exposed
mice.
Results:
Each
exposure
produced
distinct
hepatic
transcriptomes
more
tRNAs
decreased
than
increased.
Only
tRNA-Glu-TTC-1
was
reduced
all
three
exposures.
More
changes
tRFs
were
alone
PCB126
alone.
Four
tRF-3s
upregulated
both
co-exposed
mice,
suggesting
as
responsible
for
this
increase.
We
previously
reported
that
increased
Angiogenin
(ANG)
protein
generates
tRF-3s.
corresponded
positions
PCB-associated
tRAX:
m1A,
m6A,
ms2t6A,
Ψ.
Conclusions:
Overall,
different
suggest
play
an
unexplored
role
regulating
translation
liver.
Язык: Английский
Bisphenols exposure and non-alcoholic fatty liver disease: from environmental trigger to molecular pathogenesis
Frontiers in Endocrinology,
Год журнала:
2025,
Номер
16
Опубликована: Май 22, 2025
Bisphenols
(BPs),
including
bisphenol
A
(BPA)
and
its
substitutes
(BPS,
BPF),
are
ubiquitous
environmental
contaminants
with
emerging
links
to
metabolic
disorders.
This
review
synthesizes
current
evidence
on
the
role
of
BP
exposure
in
pathogenesis
non-alcoholic
fatty
liver
disease
(NAFLD),
a
global
health
crisis
affecting
25%
adults
worldwide.
Epidemiological
studies
reveal
significant
positive
associations
between
urinary/serum
levels
NAFLD
risk,
particularly
males,
maternal
correlating
transgenerational
dysfunction.
Mechanistically,
BPs
disrupt
hepatic
lipid
homeostasis
by
activating
PPAR-γ
suppressing
acid
oxidation
while
concurrently
inducing
insulin
resistance
via
impaired
IRS-1/PI3K/Akt
signaling.
Oxidative
stress,
NLRP3
inflammasome
activation,
gut-liver
axis
perturbations
further
exacerbate
steatosis
inflammation.
Co-exposure
phthalates
or
high-fat
diets
amplifies
hepatotoxicity,
highlighting
synergistic
risks.
Critically,
developmental
sex-specific
susceptibility
underscores
need
for
tailored
interventions.
We
propose
preventive
strategies
mitigate
progression,
avoidance
policy
reforms.
work
bridges
gaps
epidemiology
molecular
toxicology,
emphasizing
as
modifiable
drivers
disease.
Язык: Английский