Ukrainian journal of veterinary sciences,
Год журнала:
2023,
Номер
14(3), С. 25 - 45
Опубликована: Июль 10, 2023
To
date,
the
aetiology
and
molecular
mechanisms
of
development
fatty
hepatosis,
which
is
quite
common
in
mammals,
have
not
yet
been
sufficiently
explained.
This
pathology
requires
detailed
study
only
because
functional
disorders
liver
biliary
system,
but
also
high
probability
dangerous
complications
–
fibrosis,
cirrhosis,
or
hepatocellular
carcinoma.
The
purpose
this
was
to
determine
marker
changes
phospholipid
composition
bile
blood
rats
with
experimental
hepatosis
use
corrective
therapy.
Hepatopathology
modelled
Wistar
laboratory
by
intragastric
administration
a
4%
solution
tetracycline
hydrochloride
at
rate
0.25
g/kg
body
weight
for
seven
days.
Using
method
thin-layer
chromatography,
components
animal
were
studied.
It
found
that
during
rats,
there
decrease
total
content
bile,
mainly
due
level
phosphatidylcholine
(by
22.4-27.0%),
fraction
inositol
phosphatide
phosphatidylinositol
20.0-27.3%),
phosphatidylethanolamine
17.5-25.2%).
Conversely,
introduction
milk
phospholipids
form
dietary
supplement
“FLP-MD”
sick
animals
contributed
an
increase
levels
phosphatidylserine
67.1-99.8%,
48.6-57.6%,
38.8-60.2%,
45.6-57.4%,
sphingomyelin
30.4-46.3%.
In
such
significant
phosphatidylcholine,
phosphatidylserine,
found,
observed
after
animals.
case
using
healthy
animals,
29.3%
noted.
determination
most
sensitive
indicators
spectrum
reveals
features
processes
contributes
preclinical
tests
effectiveness
newly
created
drugs
according
established
markers
Scientific Reports,
Год журнала:
2023,
Номер
13(1)
Опубликована: Май 10, 2023
Nonalcoholic
fatty
liver
disease
(NAFLD)
encompasses
a
spectrum
of
pathologies
that
includes
steatosis,
steatohepatitis
(NASH)
and
fibrosis
is
strongly
associated
with
insulin
resistance
type
2
diabetes.
Changes
in
mitochondrial
function
are
implicated
the
pathogenesis
NAFLD,
particularly
transition
from
steatosis
to
NASH.
Mitophagy
quality
control
mechanism
allows
for
selective
removal
damaged
mitochondria
cell
via
autophagy
pathway.
While
past
work
demonstrated
negative
association
between
fat
content
rates
mitophagy,
when
changes
mitophagy
occur
during
NAFLD
whether
such
contribute
primary
endpoints
currently
poorly
defined.
We
therefore
undertook
studies
described
here
establish
alterations
as
well
determine
effects
genetic
inhibition
conditional
deletion
key
regulator,
PARKIN,
on
development
resistance,
inflammation
fibrosis.
find
loss
occurs
early
PARKIN
accelerates
onset
features.
These
observations
suggest
response
nutritional
stress
may
dysfunction
NAFLD.
Toxics,
Год журнала:
2023,
Номер
11(2), С. 135 - 135
Опубликована: Янв. 30, 2023
Autophagy
is
an
evolutionarily
conserved
cellular
system
crucial
for
homeostasis
that
protects
cells
from
a
broad
range
of
internal
and
extracellular
stresses.
decreases
metabolic
load
toxicity
by
removing
damaged
components.
Environmental
contaminants,
particularly
industrial
substances,
can
influence
autophagic
flux
enhancing
it
as
protective
response,
preventing
it,
or
converting
its
function
into
pro-cell
death
mechanism.
toxic
materials
are
also
notorious
their
tendency
to
bioaccumulate
induce
pathophysiological
vulnerability.
Many
environmental
pollutants
have
been
found
stress
which
increases
autophagy.
Increasing
autophagy
was
recently
shown
improve
resistance
reduce
genetic
damage.
Moreover,
suppressing
depleting
resources
either
toxicity,
depending
on
the
circumstances.
The
essential
process
selective
utilized
mammalian
in
order
eliminate
particulate
matter,
nanoparticles,
metals,
smoke
exposure
without
inflicting
damage
cytosolic
cigarette
aging
chief
causes
chronic
obstructive
pulmonary
disease
(COPD)-emphysema;
however,
disease’s
molecular
mechanism
poorly
known.
Therefore,
understanding
impacts
via
offers
new
approaches
risk
assessment,
protection,
preventative
actions
will
counter
harmful
effects
contaminants
human
animal
health.
Journal of Hepatocellular Carcinoma,
Год журнала:
2024,
Номер
Volume 11, С. 327 - 346
Опубликована: Фев. 1, 2024
Abstract:
Hepatocellular
carcinoma
(HCC)
stands
as
a
severe
malignant
tumor
with
profound
impact
on
overall
health,
often
accompanied
by
an
unfavorable
prognosis.
Despite
some
advancements
in
the
diagnosis
and
treatment
of
this
disease,
improving
prognosis
HCC
remains
formidable
challenge.
It
is
noteworthy
that
lipid
metabolism
plays
pivotal
role
onset,
development,
progression
cells.
Existing
research
indicates
potential
application
targeting
HCC.
This
review
aims
to
thoroughly
explore
alterations
HCC,
offering
detailed
account
advantages
associated
innovative
therapeutic
strategies
metabolism.
Targeting
holds
promise
for
potentially
enhancing
Keywords:
cholesterol,
fatty
acid,
hepatocellular
carcinoma,
uptake,
catabolism,
synthesis
Cellular
senescence
is
a
stress-induced
irreversible
cell
cycle
arrest
involved
in
tumor
suppression
and
aging.
Many
stresses,
such
as
telomere
shortening
oncogene
activation,
induce
by
damaging
nuclear
DNA.
However,
the
mechanisms
linking
DNA
damage
to
remain
unclear.
Here,
we
show
that
response
(DDR)
signaling
mitochondria
triggers
senescence.
A
genome-wide
small
interfering
RNA
screen
implicated
outer
mitochondrial
transmembrane
protein
BNIP3
induction.
We
found
phosphorylated
DDR
kinase
ataxia
telangiectasia
mutated
(ATM)
contributes
an
increase
number
of
cristae.
Stable
isotope
labeling
metabolomics
indicated
cristae
enhances
fatty
acid
oxidation
(FAO)
acetyl-coenzyme
(acetyl-CoA).
This
promotes
histone
acetylation
expression
cyclin-dependent
inhibitor
p16
Clinical and Translational Medicine,
Год журнала:
2023,
Номер
13(10)
Опубликована: Окт. 1, 2023
Enhanced
de
novo
lipogenesis
is
essential
for
hepatocellular
carcinoma
(HCC).
Abnormally
high
cullin-associated
and
neddylation-dissociated
1
(CAND1)
expression
associated
with
poor
clinical
prognosis
in
HCC.
The
SKP1-Cullin-1-F-box
(SCF)
complex
consists
of
the
SKP1,
Cullin-1
F-box
proteins
(FBPs)
performs
multiple
functions
including
adipogenesis.
SCF
was
modulated
by
CAND1,
but
Whether
how
CAND1
promotes
HCC
regulating
are
unknown.
Adipose
tissue
macrophages
(ATMs)
are
key
cellular
components
that
respond
to
nutritional
excess,
contributing
obesity-induced
inflammation
and
insulin
resistance.
However,
the
mechanisms
underlying
macrophage
polarization
recruitment
in
adipose
during
obesity
remain
unclear.
In
this
study,
we
investigated
mitophagy-dependent
metabolic
reprogramming
ATMs
identified
a
crucial
role
of
mitophagy
receptor
BNIP3
regulating
response
obesity.
Mitophagic
flux
increased
following
12
weeks
high-fat
diet
(HFD)
feeding,
with
Bnip3
levels
upregulated
HIF1A
dependent
manner,
without
affecting
other
receptors.
Macrophage-specific
bnip3
knockout
reduced
HFD-induced
improved
glucose
tolerance
sensitivity.
Mechanistically,
hypoxic
conditions
vitro
induced
HIF1A-BNIP3-mediated
glycolytic
shift
macrophages.
Furthermore,
HIF1A-BNIP3
signaling-enhanced
lipopolysaccharide-induced
pro-inflammatory
activation
These
findings
demonstrate
BNIP3-mediated
regulates
suggest
could
be
therapeutical
target
for
obesity-related
diseases.
Cancers,
Год журнала:
2023,
Номер
15(16), С. 4100 - 4100
Опубликована: Авг. 14, 2023
Cancer
shares
common
risk
factors
with
cardiovascular
diseases
such
as
dyslipidemia,
obesity
and
inflammation.
In
both
cases,
dysregulations
of
lipid
metabolism
occur,
vesicles
emerge
important
that
can
influence
carcinogenesis.
this
review,
the
role
different
lipids
known
to
be
involved
in
cancer
its
response
treatments
is
detailed.
particular,
droplets
(LDs),
initially
described
for
their
storage,
exert
multiple
functions,
from
physiological
prevention
LD
coalescence
regulation
endoplasmic
reticulum
homeostasis
pathological
involvement
tumor
progression
aggressiveness.
Analysis
LDs
highlights
importance
phosphatidylcholine
diversity
synthesis
enzymes.
many
cancers,
pathways
are
disrupted,
modifying
expression
genes
coding
metabolic
Tumor
microenvironment
conditions,
hypoxia,
types
stress
or
inflammatory
also
determinants
behavior
cells.
Therefore,
represent
therapeutic
targets
cancer,
mediators
have
emerged
potential
biomarkers
onset,
progression,
and/or
resistance.
