Journal of Cardiology and Cardiovascular Medicine,
Journal Year:
2024,
Volume and Issue:
9(1), P. 052 - 057
Published: March 6, 2024
Background:
Obesity
remains
a
global
epidemic
with
over
2.8
million
people
dying
due
to
complications
of
being
overweight
or
obese
every
year.
The
low-carbohydrate
and
high-fat
ketogenic
diet
has
rising
popularity
for
its
rapid
weight
loss
potential.
However,
most
studies
have
maximal
2-year
follow-up,
therefore
long-term
adverse
events
remain
unclear
including
the
risk
Atherosclerotic
Cardiovascular
Disease
(ASCVD).
Results:
Based
on
current
evidence
PubMed
Google
Scholar,
there
is
no
strong
indication
advantageous
loss,
lipid
profile,
mortality.
When
comparing
hypocaloric
low-fat
diet,
may
be
faster
until
6
months,
however,
this
then
appears
equivalent.
Ketogenic
diets
shown
inconsistent
Low-Density
Lipoprotein
(LDL)
changes;
perhaps
from
different
saturated
fat
intake,
dietary
adherence,
genetics.
Case
reports
2-4-fold
elevation
in
LDL
Familial
hypercholesterolaemic
patients
which
mostly
reversed
upon
discontinuation.
There
also
concern
about
possible
increased
ASCVD
mortality:
low
(<
40%)
carbohydrate
intake
been
associated
mortality,
high
fats,
animal
product
consumption
can
increase
trimethylamine
N-oxide,
cardioprotective
foods
are
likely
minimally
ingested.
Conclusion:
short-term
positive
effects
larger
reductions.
by
2
years
significant
differences
cardiometabolic
markers.
Therefore,
raises
question,
excluding
those
who
critical
need
lose
fast,
worth
potentially
higher
risks
mortality
while
further
awaited?
Frontiers in Oncology,
Journal Year:
2025,
Volume and Issue:
15
Published: Jan. 29, 2025
Metformin
(MET)
is
a
commonly
used
drug
for
the
treatment
of
type
2
diabetes
in
department
endocrinology.
In
recent
years,
due
to
few
clinically
effective
options
including
glioma,
some
scholars
have
proposed
possibility
metformin
and
studies
shown
that
has
certain
inhibitory
effect
on
this
tumor.
This
review
explores
multiple
mechanisms
through
which
exerts
its
antitumor
effects,
focusing
signaling
pathways
such
as
AMPK/mTOR,
ferroptosis,
autophagy,
apoptosis
chloride
ion
channels
(CLIC1).
Metformin’s
inhibition
glioma
proliferation
involves
complex
cellular
processes,
mitochondrial
dysfunction,
increased
reactive
oxygen
species
(ROS)
production,
modulation
immune
responses.
Additionally,
affects
stem
cells
by
inhibiting
key
pathways,
STAT3,
mTOR,
AKT,
altering
tumor
microenvironment.
While
preclinical
suggest
enhances
radiosensitivity
reduces
recurrence,
clinical
application
remains
early
stages,
with
further
needed
optimize
dosing
regimens
understand
full
therapeutic
potential.
provides
comprehensive
analysis
metformin’s
molecular
highlights
potential
novel
strategy,
especially
treatment-resistant
gliomas.
Phytotherapy Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 14, 2025
ABSTRACT
Non‐alcoholic
fatty
liver
disease
(NAFLD)
is
a
progressive
condition
with
limited
effective
treatments.
This
study
investigated
the
therapeutic
effects
of
Aurantio‐obtusin
(AO),
bioactive
compound
from
Cassiae
Semen
,
on
obesity‐associated
NAFLD.
An
obesity‐related
NAFLD
model
was
established
in
ApoE
−/−
mice
fed
high‐fat
diet
(HFD)
for
24
weeks,
AO
administered
during
last
16
weeks.
Mouse
body
weight,
adipose
tissue
weights,
serum
lipid
levels,
hepatic
steatosis,
inflammatory
damage,
and
colonic
barrier
integrity
were
evaluated.
Gut
microbial
communities
metabolic
profiles
analyzed
using
16S
rRNA
sequencing
untargeted
metabolomics.
Hepatic
metabolism‐related
gene
expression
assessed
molecular
biology
techniques.
treatment
significantly
ameliorated
HFD‐induced
adiposity,
hyperlipidemia,
symptoms.
It
preserved
intestinal
integrity,
modulated
gut
composition
by
enriching
beneficial
taxa,
improved
profiles.
favorably
adjusted
metabolism
upregulating
PPARα
CPT1A
while
downregulating
SREBP1,
FASN,
SCD1.
Correlation
analysis
revealed
significant
associations
among
composition,
metabolites,
indicators.
AO's
benefits
might
be
attributed
to
its
ability
modulate
community
profile,
enhance
function,
regulate
expression.
presents
promising
agent
NAFLD,
warranting
further
investigation
into
potential
clinical
applications.
Drug Metabolism and Disposition,
Journal Year:
2024,
Volume and Issue:
52(8), P. 754 - 764
Published: Feb. 1, 2024
The
mammalian
gut
microbiota
plays
diverse
and
essential
roles
in
modulating
host
physiology.
Key
mediators
determining
the
outcome
of
microbiota-host
interactions
are
small
molecule
metabolites
produced
by
microbiota.
liver
is
organ
massively
exposed
to
microbial
metabolites,
it
serves
as
nexus,
maintaining
healthy
between
host.
At
same
time,
primary
target
harmful
metabolites.
This
review
provides
an
up-to-date
list
identified
increase
or
decrease
susceptibility
APAP-induced
injury.
Signaling
pathways
molecular
factors
involved
progression
hepatotoxicity
well-established,
we
propose
that
mouse
model
excellent
system
for
uncovering
previously
unknown
function.
Moreover,
envision
alter
likely
have
broader
implications
other
diseases.
Significance
Statement
overview
recent
discoveries
from
investigating
whether
how
modulates
It
focuses
on
bacterial
interaction
liver.
also
illustrates
utility
injury
a
identify
with
biological
Scientifica,
Journal Year:
2024,
Volume and Issue:
2024(1)
Published: Jan. 1, 2024
Since
its
discovery,
numerous
studies
have
shown
the
role
of
microbiota
in
well‐being
and
disease.
The
gut
represents
an
essential
factor
that
plays
a
multidirectional
affects
not
just
but
also
other
parts
body,
including
brain,
endocrine
system,
humoral
immune
metabolic
pathways,
as
well
host‐microbiome
interactions.
Through
comprehensive
analysis
existing
literature
using
desktop
research
methodology,
this
review
elucidates
mechanisms
by
which
dysbiosis
contributes
to
dysfunction,
obesity,
dyslipidaemia,
hypertension,
atherosclerosis,
hyperuricemia,
hyperglycaemia.
Furthermore,
it
examines
bidirectional
communication
pathways
between
host
metabolism,
highlighting
microbial‐derived
metabolites,
modulation,
barrier
integrity
shaping
homeostasis.
Importantly,
identifies
promising
therapeutic
strategies
targeting
potential
interventions
for
syndrome,
probiotics,
prebiotics,
symbiotics,
dietary
modifications,
faecal
transplantation.
By
delineating
interactions
only
advances
our
understanding
disease
pathophysiology
underscores
innovative
microbiota‐based
mitigate
global
burden
syndrome
associated
complications.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Sept. 16, 2024
The
human
microbiome
has
recently
emerged
as
a
focal
point
in
cancer
research,
specifically
anti-tumor
immunity,
immunotherapy,
and
chemotherapy.
This
review
explores
microbial-derived
metabolites,
emphasizing
their
crucial
roles
shaping
fundamental
aspects
of
treatment.
Metabolites
such
short-chain
fatty
acids
(SCFAs),
Trimethylamine
N-Oxide
(TMAO),
Tryptophan
take
the
spotlight,
underscoring
diverse
origins
functions
profound
impact
on
host
immune
system.
focus
is
SCFAs’
remarkable
ability
to
modulate
responses,
reduce
inflammation,
enhance
immunity
within
intricate
tumor
microenvironment
(TME).
critically
evaluates
TMAO,
intricately
tied
dietary
choices
gut
microbiota
composition,
assessing
its
implications
for
susceptibility,
progression,
immunosuppression.
Additionally,
involvement
tryptophan
other
amino
acid
metabolites
responses
discussed,
highlighting
influence
checkpoints,
immunosuppression,
immunotherapy
effectiveness.
examination
extends
dynamic
interaction
with
chemotherapy,
potential
alter
treatment
protocols
optimize
outcomes
patients.
A
comprehensive
understanding
role
therapy
attained
by
exploring
impacts
drug
metabolism,
therapeutic
resistance
development.
In
conclusion,
this
underscores
pivotal
contributions
regulating
chemotherapy
outcomes.
By
illuminating
interactions
between
these
therapy,
article
enhances
our
biology,
paving
way
development
more
effective
options
ongoing
battle
against
cancer.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(19), P. 10397 - 10397
Published: Sept. 27, 2024
Cardiovascular
disease
is
the
main
cause
of
mortality
in
industrialized
countries,
with
over
500
million
people
affected
worldwide.
In
this
work,
roles
low-molecular-weight
metabolites
originating
from
gut
microbiome,
such
as
short-chain
fatty
acids,
hydrogen
sulfide,
trimethylamine,
phenylacetic
acid,
secondary
bile
indoles,
different
gases,
neurotransmitters,
vitamins,
and
complex
lipids,
are
discussed
relation
to
their
CVD-promoting
or
preventing
activities.
Molecules
mixed
microbial
human
hepatic
origin,
trimethylamine
N-oxide
phenylacetylglutamine,
also
presented.
Finally,
dietary
agents
cardioprotective
effects,
probiotics,
prebiotics,
mono-
poly-unsaturated
carotenoids,
polyphenols,
discussed.
A
special
emphasis
given
microbiota-modulating
properties.
Eurasian Journal of Medicine,
Journal Year:
2024,
Volume and Issue:
55(S1), P. 21 - 26
Published: Feb. 28, 2024
Trimethylamine
N-oxide
(TMAO),
the
oxidized
form
of
trimethylamine
(TMA),
was
previously
thought
to
be
a
waste
product
but
is
now
considered
an
important
risk
factor
for
cardiovascular
disease
(CVD)
and
its
comorbidities.
Foods
or
supplements
containing
choline
carnitine
are
major
precursors
TMA
in
diet
metabolized
by
gut
microbiota.
produced
through
oxidation
this
compound
flavin-containing
monooxygenase
(FMO)
liver.
The
organ
responsible
removal
TMAO
from
body
fluids
kidneys.
Therefore,
plasma
levels
influenced
multiple
complex
factors,
especially
amount
dietary
sources
diet,
dominant
genera
microbiota,
FMO3
enzyme
activity,
kidney
functions.
Among
these,
quantity
microbiota
can
modifiable
factors.
However,
discussions
continue
regarding
how
reach
pathological
their
role
(consequence
cause)
CVD.
This
review
presents
current
scientific
evidence
on
relationship
underlying
mechanisms
between
CVD
provides
overview
association
with
such
as
precursors,
sources,
Maternal
obesity
and/or
Western
diet
(WD)
is
associated
with
increased
risk
of
metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD)
in
offspring,
driven,
part,
by
dysregulation
the
early
life
microbiome.
Here,
using
a
mouse
model
WD-induced
maternal
obesity,
we
demonstrate
that
exposure
to
disordered
microbiome
from
WD-fed
dams
suppressed
circulating
levels
endogenous
ligands
aryl
hydrocarbon
receptor
(AHR;
indole,
indole-3-acetate)
and
TMAO
(a
product
AHR-mediated
transcription),
as
well
hepatic
expression
Il10
(an
AHR
target),
offspring
at
3
weeks
age.
This
signature
was
recapitulated
fecal
microbial
transfer
pregnant
chow-fed
germ-free
(GF)
lactating
following
parturition,
reduced
abundance
Lactobacillus
GF
offspring.
Further,
downregulated
myeloid
cells
LPS-stimulated
bone
marrow-derived
macrophages
(BMDM)
adult
suggestive
hypo-responsive,
or
tolerant,
innate
immune
response.
BMDMs
mice
lacking
exhibited
similar
tolerogenic
response,
including
diminished
Il10.
Overall,
our
study
shows
WD
alters
metabolites
affect
signaling,
potentially
contributing
hypo-responsiveness
progression
MASLD,
highlights
impact
gut
dysbiosis
on
metabolism.
Further
investigations
are
warranted
elucidate
complex
interplay
between
diet,
function,
development
neonatal
tolerance
potential
therapeutic
interventions
targeting
these
pathways.