Communications Biology,
Journal Year:
2024,
Volume and Issue:
7(1)
Published: Feb. 16, 2024
Abstract
The
Ketogenic
Diet
(KD)
improves
memory
and
longevity
in
aged
C57BL/6
mice.
We
tested
7
months
KD
vs.
control
diet
(CD)
the
mouse
Alzheimer’s
Disease
(AD)
model
APP/PS1.
significantly
rescued
Long-Term-Potentiation
(LTP)
to
wild-type
levels,
not
by
changing
Amyloid-β
(Aβ)
levels.
KD’s
‘main
actor’
is
thought
be
Beta-Hydroxy-butyrate
(BHB)
whose
levels
rose
CD
mice,
BHB
itself
LTP
APP/PS1
hippocampi.
6
most
significant
pathways
induced
brains
RNAseq
all
related
Synaptic
Plasticity.
increases
synaptic
plasticity
enzymes
p-ERK
p-CREB
both
sexes,
of
brain-derived
neurotrophic
factor
(BDNF)
females.
suggest
rescues
through
BHB’s
enhancement
plasticity.
falls
Mild-Cognitive
Impairment
(MCI)
human
AD.
BHB,
because
they
are
an
approved
supplement
respectively,
may
therapeutically
translationally
relevant
MCI
phase
Disease.
Nutrients,
Journal Year:
2021,
Volume and Issue:
13(5), P. 1654 - 1654
Published: May 13, 2021
Considering
the
lack
of
a
comprehensive,
multi-faceted
overview
ketogenic
diet
(KD)
in
relation
to
health
issues,
we
compiled
evidence
related
use
its
impact
on
microbiome,
epigenome,
diabetes,
weight
loss,
cardiovascular
health,
and
cancer.
The
KD
could
potentially
increase
genetic
diversity
microbiome
ratio
Bacteroidetes
Firmicutes.
epigenome
might
be
positively
affected
by
since
it
creates
signaling
molecule
known
as
β-hydroxybutyrate
(BHB).
has
helped
patients
with
diabetes
reduce
their
HbA1c
need
for
insulin.
There
is
suggest
that
can
help
visceral
adiposity,
appetite
control.
also
suggests
eating
high-fat
improves
lipid
profiles
lowering
low-density
lipoprotein
(LDL),
increasing
high-density
(HDL),
triglycerides
(TG).
Due
Warburg
effect,
used
an
adjuvant
treatment
starve
cancer
cells,
making
them
more
vulnerable
chemotherapy
radiation.
potential
positive
impacts
each
these
areas
warrant
further
analysis,
improved
studies,
well-designed
randomized
controlled
trials
illuminate
therapeutic
possibilities
provided
this
dietary
intervention.
Frontiers in Nutrition,
Journal Year:
2021,
Volume and Issue:
8
Published: July 16, 2021
Very-low-carbohydrate
ketogenic
diets
have
been
long
used
to
reduce
seizure
frequency
and
more
recently
promoted
for
a
variety
of
health
conditions,
including
obesity,
diabetes,
liver
disease.
Ketogenic
may
provide
short-term
improvement
aid
in
symptom
management
some
chronic
diseases.
Such
affect
diet
quality,
typically
increasing
intake
foods
linked
disease
risk
decreasing
found
be
protective
epidemiological
studies.
This
review
examines
the
effects
on
common
diseases,
as
well
their
impact
quality
possible
risks
associated
with
use.
Given
often-temporary
improvements,
unfavorable
dietary
intake,
inadequate
data
demonstrating
long-term
safety,
most
individuals,
outweigh
benefits.
Cell Reports,
Journal Year:
2021,
Volume and Issue:
35(10), P. 109212 - 109212
Published: June 1, 2021
Obesity
is
an
established
risk
factor
for
cancer
in
many
tissues.
In
the
mammalian
intestine,
a
pro-obesity
high-fat
diet
(HFD)
promotes
regeneration
and
tumorigenesis
by
enhancing
intestinal
stem
cell
(ISC)
numbers,
proliferation,
function.
Although
PPAR
(peroxisome
proliferator-activated
receptor)
nuclear
receptor
activity
has
been
proposed
to
facilitate
these
effects,
their
exact
role
unclear.
Here
we
find
that,
loss-of-function
vivo
models,
PPARα
PPARδ
contribute
HFD
response
ISCs.
Mechanistically,
both
PPARs
do
so
robustly
inducing
downstream
fatty
acid
oxidation
(FAO)
metabolic
program.
Pharmacologic
genetic
disruption
of
CPT1A
(the
rate-controlling
enzyme
mitochondrial
FAO)
blunts
phenotype
Furthermore,
inhibition
dampens
pro-tumorigenic
consequences
on
early
tumor
incidence
progression.
These
findings
demonstrate
that
HFD-activated
FAO
program
creates
therapeutic
opportunity
counter
effects
ISCs
tumorigenesis.
Biomolecules,
Journal Year:
2021,
Volume and Issue:
11(3), P. 402 - 402
Published: March 9, 2021
3-hydroxybutyrate
(3-HB)
as
a
very
important
metabolite
occurs
in
animals,
bacteria
and
plants.
It
is
well
known
that
3-HB
formed
product
of
the
normal
metabolism
fatty
acid
oxidation
can
therefore
be
used
an
energy
source
absence
sufficient
blood
glucose.
In
microorganisms,
mainly
serves
substrate
for
synthesis
polyhydroxybutyrate,
which
reserve
material.
Recent
studies
show
plants,
acts
regulatory
molecule
most
likely
influences
expression
genes
involved
DNA
methylation,
thereby
altering
methylation
levels.
Additionally,
not
only
intermediate
metabolite,
but
also
influence
gene
expression,
lipid
metabolism,
neuronal
function,
overall
metabolic
rate.
Some
these
effects
are
direct
itself,
while
others
indirect
effects,
regulated
by
metabolites
into
converted.
One
functions
inhibition
activity
histone
deacetylases
thus
epigenetic
regulation
many
genes.
Due
to
number
this
compound,
it
shows
promising
therapeutic
properties.
Liver International,
Journal Year:
2021,
Volume and Issue:
41(10), P. 2249 - 2268
Published: July 30, 2021
Lifestyle
represents
the
most
relevant
factor
for
non-alcoholic
fatty
liver
disease
(NAFLD)
as
hepatic
manifestation
of
metabolic
syndrome.
Although
a
tremendous
body
clinical
and
preclinical
data
on
effectiveness
dietary
lifestyle
interventions
exist,
complexity
this
topic
makes
firm
evidence-based
recommendations
nutrition
exercise
in
NAFLD
difficult.
The
aim
review
is
to
guide
readers
through
labyrinth
recent
scientific
findings
diet
steatohepatitis
(NASH),
summarizing
"obvious"
holistic
manner
simultaneously
highlighting
stimulating
aspects
translational
research
"beyond
obvious".
Specifically,
importance
calorie
restriction
regardless
composition
evidence
from
low-carbohydrate
diets
target
incidence
severity
are
discussed.
aspect
ketogenesis-potentially
achieved
via
intermittent
restriction-seems
be
central
these
warranting
further
investigation.
Interactions
with
gut
microbiota
individual
genetic
background
need
comprehensively
understood
order
develop
personalized
concepts
strategies
patients
NAFLD/NASH.
Journal of Molecular and Cellular Cardiology,
Journal Year:
2022,
Volume and Issue:
167, P. 17 - 31
Published: March 21, 2022
Sodium
glucose
cotransporter
2
inhibitors
(SGLT2i)
constitute
a
promising
drug
treatment
for
heart
failure
patients
with
either
preserved
or
reduced
ejection
fraction.
Whereas
SGLT2i
were
originally
developed
to
target
SGLT2
in
the
kidney
facilitate
glucosuria
diabetic
patients,
it
is
becoming
increasingly
clear
that
these
drugs
also
have
important
effects
outside
of
kidney.
In
this
review
we
summarize
literature
on
cardiac
SGLT2i,
focussing
pro-inflammatory
and
oxidative
stress
processes,
ion
transport
mechanisms
controlling
sodium
calcium
homeostasis
metabolic/mitochondrial
pathways.
These
are
particularly
as
disturbances
pathways
result
endothelial
dysfunction,
diastolic
stiffness,
arrhythmias
together
contribute
failure.
We
findings
support
concept
directly
beneficially
interfere
inflammation,
stress,
ionic
homeostasis,
metabolism
within
cell.
However,
given
very
low
levels
cells,
evidence
suggests
SGLT2-independent
class
likely
occurs
via
off-target
myocardium.
Thus,
while
there
still
much
be
understood
about
various
factors
which
determine
how
affect
research
clearly
demonstrates
direct
exist,
albeit
mediated
pathways,
may
play
role
explaining
beneficial