Deleted Journal,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 13, 2025
Abstract
Metabolic
diseases,
including
obesity,
diabetes,
and
metabolic‐associated
fatty
liver
disease
(MAFLD),
are
increasingly
common
worldwide,
posing
a
significant
public
health
challenge.
Recent
research
has
revealed
complex
interplay
between
these
metabolic
disorders
interferon
(IFN)
immune
responses.
As
key
regulators,
interferons
coordinate
the
host's
defense
against
viral
infections
essential
for
maintaining
homeostasis.
However,
dysregulation
can
significantly
disrupt
IFN
signaling
pathways,
affecting
intensity
efficiency
of
Conversely,
alterations
in
influence
onset
progression
diseases.
This
review
explores
mechanisms
by
which
diseases
modulate
responses,
focusing
on
how
MAFLD
alter
signaling.
Additionally,
we
examine
implications
changes
responses
By
synthesizing
current
research,
this
aims
to
elucidate
offering
insights
future
clinical
applications
field
IFN‐related
JHEP Reports,
Journal Year:
2024,
Volume and Issue:
6(12), P. 101185 - 101185
Published: Aug. 9, 2024
Metabolic
dysfunction-associated
steatotic
liver
disease/steatohepatitis
(MASLD/MASH)
is
recognised
as
a
metabolic
disease
characterised
by
excess
intrahepatic
lipid
accumulation
due
to
overflow
and
synthesis,
alongside
impaired
oxidation
and/or
export
of
these
lipids.
But
where
do
lipids
come
from?
The
main
pathways
related
hepatic
are
European Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
54(7)
Published: Feb. 21, 2024
The
role
of
insulin
resistance
in
hepatic
fibrosis
Metabolic
dysfunction-Associated
SteatoHepatitis
(MASH)
remains
unclear.
Carcinoembryonic
Antigen-related
Cell
Adhesion
Molecule1
protein
(CEACAM1)
promotes
clearance
to
maintain
sensitivity
and
repress
de
novo
lipogenesis,
as
bolstered
by
the
development
steatohepatitis
AlbuminCre
+
Cc1
Molecules,
Journal Year:
2024,
Volume and Issue:
29(7), P. 1494 - 1494
Published: March 27, 2024
Detailed
investigation
of
the
lipidome
remodeling
upon
normal
weight
conditions,
obesity,
or
loss,
as
well
influence
physical
activity,
can
help
to
understand
mechanisms
underlying
dyslipidemia
in
metabolic
conditions
correlated
emergence
and
progression
non-alcoholic
fatty
liver
disease
(NAFLD).
C57BL/6
male
mice
were
fed
a
diet
(ND)
high-fat
(HFD)
for
20
weeks.
Subgroups
within
group
underwent
different
interventions:
some
engaged
exercise
(HFDex),
others
subjected
loss
(WL)
by
changing
from
HFD
ND,
combination
(WLex)
during
final
8
weeks
20-week
feeding
period.
To
support
our
understanding,
not
only
tissue-specific
lipid
but
also
cross-talk
between
tissues
their
impact
on
systemic
regulation
metabolism
are
essential.
Exercise
loss-induced
specific
adaptations
visceral
adipose
tissue
lipidomes
explored
UPLC–TOF–MS/MS
untargeted
lipidomics
methodology.
Lipidomic
signatures
ND
HFD-fed
undergoing
compared
with
animals
without
exercise.
Several
classes
identified
contributing
factors
discrimination
groups
multivariate
analysis
models,
such
glycerolipids,
glycerophospholipids,
sphingolipids,
acids,
respect
samples,
whereas
triglycerides
class
tissue.
Lipids
found
be
dysregulated
related
well-established
pathways
involved
biosynthesis
PC,
PE,
TG
metabolism.
These
show
reversing
trend
back
basic
levels
when
change
after
12
weeks,
exercise,
though
cases
it
slightly
enhances
trend,
is
clear.
Deleted Journal,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 13, 2025
Abstract
Metabolic
diseases,
including
obesity,
diabetes,
and
metabolic‐associated
fatty
liver
disease
(MAFLD),
are
increasingly
common
worldwide,
posing
a
significant
public
health
challenge.
Recent
research
has
revealed
complex
interplay
between
these
metabolic
disorders
interferon
(IFN)
immune
responses.
As
key
regulators,
interferons
coordinate
the
host's
defense
against
viral
infections
essential
for
maintaining
homeostasis.
However,
dysregulation
can
significantly
disrupt
IFN
signaling
pathways,
affecting
intensity
efficiency
of
Conversely,
alterations
in
influence
onset
progression
diseases.
This
review
explores
mechanisms
by
which
diseases
modulate
responses,
focusing
on
how
MAFLD
alter
signaling.
Additionally,
we
examine
implications
changes
responses
By
synthesizing
current
research,
this
aims
to
elucidate
offering
insights
future
clinical
applications
field
IFN‐related
