EBioMedicine,
Journal Year:
2023,
Volume and Issue:
94, P. 104714 - 104714
Published: July 16, 2023
Disturbed
hepatic
energy
metabolism
contributes
to
non-alcoholic
fatty
liver
(NAFLD),
but
the
development
of
changes
over
time
and
obesity-
or
diabetes-related
mechanisms
remained
unclear.Two-day
old
male
C57BL/6j
mice
received
streptozotocin
(STZ)
placebo
(PLC)
then
high-fat
(HFD)
regular
chow
diet
(RCD)
from
week
4
(W4)
either
W8
W16,
yielding
control
[CTRL
=
PLC
+
RCD],
diabetes
[DIAB
STZ
obesity
[OBES
HFD]
steatohepatitis
[NASH
models.
Mitochondrial
respiration
was
measured
by
high-resolution
respirometry
insulin-sensitive
glucose
hyperinsulinemic-euglycemic
clamps
with
stable
isotope
dilution.NASH
showed
higher
steatosis
NAFLD
activity
already
at
fibrosis
W16
(all
p
<
0.01
vs
CTRL).
Ballooning
increased
in
DIAB
NASH
(p
At
insulin
sensitivity
47%,
58%
75%
lower
DIAB,
OBES
0.001
Hepatic
uncoupled
acid
oxidation
(FAO)-associated
reduced
W8,
doubled
CTRL)
correlated
biomarkers
unfolded
protein
response
(UPR),
oxidative
stress
expression
certain
enzymes
(acetyl-CoA
carboxylase
2,
Acc2;
carnitine
palmitoyltransferase
I,
Cpt1a).
Tricarboxylic
cycle
(TCA)-driven
0.0001
CTRL),
which
positively
genes
related
lipolysis.Hepatic
mitochondria
adapt
various
metabolic
challenges
increasing
FAO-driven
respiration,
is
linked
dysfunctional
UPR,
systemic
stress,
resistance
altered
lipid
metabolism.
In
a
model,
TCA-linked
reflected
mitochondrial
adaptation
greater
turnover.Funding
bodies
that
contributed
this
study
were
listed
acknowledgements
section.
Current Obesity Reports,
Journal Year:
2023,
Volume and Issue:
12(3), P. 191 - 206
Published: July 5, 2023
To
summarize
experimental
and
clinical
evidence
on
the
association
between
tumor
necrosis
factor-α
(TNF-α)
nonalcoholic
fatty
liver
disease
(NAFLD)
discuss
potential
treatment
considerations.Experimental
suggests
that
TNF-α
is
a
cytokine
with
critical
role
in
pathogenesis
of
NAFLD.
Although,
production
may
be
an
early
event
during
course
(NAFL),
play
more
substantial
steatohepatitis
(NASH)
NAFLD-associated
fibrosis.
Moreover,
potentiate
hepatic
insulin
resistance,
thus
interconnecting
inflammatory
metabolic
signals
possibly
contributing
to
development
NAFLD-related
comorbidities,
including
cardiovascular
disease,
hepatocellular
carcinoma,
extra-hepatic
malignancies.
In
terms,
probably
associated
severity
NAFLD;
circulating
gradually
increases
from
controls
patients
NAFL,
then,
NASH.
Given
this
association,
various
therapeutic
interventions
(obeticholic
acid,
peroxisome
proliferator-activated
receptors,
sodium-glucose
co-transporter
2
inhibitors,
glucagon-like
peptide-1
receptor
agonists,
probiotics,
synbiotics,
rifaximin,
vitamin
E,
pentoxifylline,
ursodeoxycholic
fibroblast
growth
factor-21,
n-3
polyunsaturated
acids,
statins,
angiotensin
blockers)
have
been
evaluated
for
their
effect
Interestingly,
anti-TNF
biologics
shown
favorable
effects,
which
open
possible
window
management
advanced
The
key
pathogenic
NAFLD
warrants
further
investigation
important
diagnostic
implications.
Nutrients,
Journal Year:
2021,
Volume and Issue:
13(8), P. 2590 - 2590
Published: July 28, 2021
Plasma
free
fatty
acid
(FFA)
concentration
is
elevated
in
obesity,
insulin
resistance
(IR),
non-alcoholic
liver
disease
(NAFLD),
type
2
diabetes
(T2D),
and
related
comorbidities
such
as
cardiovascular
(CVD).
Furthermore,
experimentally
manipulating
plasma
FFA
the
laboratory
setting
modulates
metabolic
markers
of
these
processes.
In
this
article,
evidence
presented
indicating
that
a
risk
factor.
Elevations
can
promote
ectopic
lipid
deposition,
IR,
well
vascular
cardiac
dysfunction.
Typically,
results
from
accelerated
adipose
tissue
lipolysis,
caused
by
high
mass,
adrenal
hormones,
or
other
physiological
stressors.
Reducing
an
individual’s
postabsorptive
postprandial
expected
to
improve
health.
Lifestyle
change
could
provide
significant
opportunity
for
reduction.
Various
factors
impact
concentration,
chronic
restriction
dietary
energy
intake
weight
loss,
exercise,
sleep
quality
quantity,
cigarette
smoking.
review,
consideration
given
multiple
which
lead
elevation
subsequent
disruption
From
considering
variety
medical
conditions
lifestyle
factors,
it
becomes
clear
modifiable
factor
disease.
Journal of Gastroenterology and Hepatology,
Journal Year:
2020,
Volume and Issue:
36(6), P. 1497 - 1507
Published: Nov. 21, 2020
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
one
of
the
most
common
causes
hepatic
disorders.
It
represents
a
wide
range
chronic
diseases
in
patients
with
no
history
significant
alcohol
consumption,
starting
simple
steatosis
and
progressing
towards
non-alcoholic
steatohepatitis,
cirrhosis,
ultimately
hepatocellular
carcinoma.
NAFLD
usually
associated
type
2
diabetes
mellitus,
dyslipidemia,
metabolic
syndrome,
obesity.
This
has
mostly
been
studied
obese
individuals;
however,
it
widely
reported
among
lean/non-obese
population
recent
years.
The
pathogenesis
non-obese
various
genetic
predispositions,
particularly
patatin-like
phospholipase
domain-containing
protein
3
G
allele
polymorphism,
which
results
accumulation
triglyceride
resistance
to
insulin.
Additionally,
dietary
factors
such
as
high
fructose
consumption
seem
play
substantial
role
pathology
NAFLD.
Although
there
not
enough
evidence
on
treatment
patients,
standard
approach
advise
altering
one's
lifestyle
order
diminish
visceral
adiposity.
Dietary
modification,
weight
loss,
increased
physical
activity
are
highly
recommended.
We
aimed
review
summarize
existing
information
prevalence,
pathogenesis,
diagnosis,
according
latest
literature.
EBioMedicine,
Journal Year:
2021,
Volume and Issue:
73, P. 103661 - 103661
Published: Oct. 28, 2021
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
affecting
more
people
globally.
Indeed,
NAFLD
a
spectrum
of
metabolic
dysfunctions
that
can
progress
to
hepatocellular
carcinoma
(NAFLD-HCC).
This
development
occur
in
non-cirrhotic
and
thus,
often
lack
clinical
surveillance.
The
aim
this
study
was
develop
non-invasive
surveillance
method
for
NAFLD-HCC.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(13), P. 6900 - 6900
Published: June 27, 2021
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
a
major
public
health
problem
worldwide.
NAFLD
(both
simple
steatosis
and
steatohepatitis)
characterized
by
alterations
in
hepatic
lipid
metabolism,
which
may
lead
to
the
development
of
severe
complications
including
cirrhosis
hepatocellular
carcinoma.
Thus,
an
exhaustive
examination
disorders
patients
much
needed.
Mass
spectrometry-based
lipidomics
platforms
allow
for
in-depth
analysis
number
human
diseases,
NAFLD.
This
review
summarizes
current
research
on
associated
with
related
complications,
special
emphasis
changes
long-chain
short-chain
acids
levels
both
serum
tissue,
as
well
expression
genes
encoding
enzymes
catalyzing
interconversions.
Frontiers in Endocrinology,
Journal Year:
2021,
Volume and Issue:
12
Published: Oct. 11, 2021
Nonalcoholic
fatty
liver
disease
(NAFLD)
includes
a
spectrum
of
disorders,
from
to
nonalcoholic
steatohepatitis
(NASH),
cirrhosis,
and
hepatocellular
carcinoma.
Compared
with
liver,
NASH
is
characterized
by
increased
injury
inflammation,
in
which
liver-infiltrating
immune
cells,
neutrophil
infiltration
as
hallmark
NASH,
play
critical
role
promoting
the
progression
NASH.
Neutrophils
are
first
responders
infection
various
tissues,
establishing
line
defense
through
multiple
mechanisms
such
phagocytosis,
cytokine
secretion,
reactive
oxygen
species
production,
extracellular
trap
formation;
however,
their
roles
pathogenesis
remain
obscure.
The
current
review
summarizes
neutrophils
that
facilitate
involvement
inflammation
resolution
during
pathogenesis.
notion
potential
therapeutic
targets
for
treatment
also
discussed.
Molecules,
Journal Year:
2022,
Volume and Issue:
27(3), P. 858 - 858
Published: Jan. 27, 2022
Non-alcoholic
fatty
liver
disease
(NAFLD)
embraces
several
forms
of
disorders
involving
fat
disposition
in
hepatocytes
ranging
from
simple
steatosis
to
the
severe
stage,
namely,
non-alcoholic
steatohepatitis
(NASH).
Recently,
experimental
vivo
animal
models
for
NAFLD/NASH
have
been
established.
However,
no
reproducible
model
displays
full
spectrum
pathophysiological,
histological,
molecular,
and
clinical
features
associated
with
human
progression.
Although
methionine-choline-deficient
(MCD)
diet
high-fat
(HFD)
can
mimic
histological
metabolic
abnormalities
disease,
respectively,
molecular
signaling
pathways
are
extremely
important
understanding
pathogenesis
disease.
This
review
aimed
assess
differences
gene
expression
patterns
progression
among
most
common
dietary
models,
i.e.,
HFD-
MCD
diet-fed
animals.
Studies
showed
that
HFD
could
induce
either
up-
or
downregulation
genes
proteins
involved
lipid
metabolism,
inflammation,
oxidative
stress,
fibrogenesis
pathways.
Interestingly,
spontaneously
develop
fibrosis
within
two
four
weeks
has
significant
effects
on
encode
enzymes
pathway.
such
were
found
occur
after
24
insulin
resistance
but
appear
cause
less
fibrosis.
In
conclusion,
assessing
abnormal
caused
by
different
types
provides
valuable
information
regarding
mechanisms
predicts
profiling
studies
concerning
genetic
variants
development
should
be
conducted.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(1), P. 498 - 498
Published: Jan. 2, 2022
Non-alcoholic
steatohepatitis
(NASH)
is
characterized
by
steatosis,
lobular
inflammation,
and
enlargement
of
the
diameter
hepatocytes
(ballooning
hepatocytes),
with
or
without
fibrosis.
It
affects
20%
patients
non-alcoholic
fatty
liver
disease
(NAFLD).
Due
to
dysfunction
numerous
metabolic
changes
that
commonly
accompany
condition
(obesity,
insulin
resistance,
type
2
diabetes,
syndrome),
secretion
organokines
modified,
which
may
contribute
pathogenesis
progression
disease.
In
this
sense,
study
aimed
perform
a
review
role
in
NASH.
Thus,
combining
descriptors
such
as
NASH,
organokines,
oxidative
stress,
dyslipidemia,
search
was
carried
out
EMBASE,
MEDLINE-PubMed,
Cochrane
databases
articles
published
last
ten
years.
Insulin
inflammation
mitochondrial
dysfunction,
fructose,
intestinal
microbiota
were
factors
identified
participating
genesis
Changes
pattern
(adipokines,
myokines,
hepatokines,
osteokines)
directly
indirectly
aggravating
compromise
homeostasis.
further
studies
involving
skeletal
muscle,
adipose,
bone,
tissue
endocrine
organs
are
essential
better
understand
modulation
involved
NASH
advance
treatment