Sleep Medicine Reviews,
Journal Year:
2022,
Volume and Issue:
62, P. 101594 - 101594
Published: Feb. 1, 2022
Poor
sleep
habits
are
associated
with
increased
risk
of
developing
type
2
diabetes.
In
this
review
and
meta-analysis,
we
aimed
to
investigate
the
effects
manipulation
on
markers
insulin
sensitivity
from
randomized,
controlled
trials.
Sleep
was
defined
as
reduction
in
duration,
quality,
circadian
misalignment.
A
systematic
literature
search
conducted
three
databases
resulted
35
eligible
articles.
The
studies
included
interventions
restriction
(26
studies),
slow
wave
suppression
rapid
eye
movement
disturbance
(2
fragmentation
misalignment
(5
studies).
meta-analysis
21
studies.
reduced
assessed
by
oral
or
intravenous
glucose
tolerance
test
homeostatic
model
assessment
resistance.
Whole-body
also
after
short
when
measured
hyperinsulinemic
euglycemic
clamp,
but
peripheral
not
affected.
addition,
negatively
affected
sensitivity,
while
had
no
effect.
summary,
indicated
that
timing
essential
for
metabolic
function
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: March 15, 2024
Sleep
is
a
modifiable
behavior
that
can
be
targeted
in
interventions
aimed
at
promoting
healthy
aging.
This
study
aims
to
(i)
identify
the
sleep
duration
trend
US
adults;
(ii)
investigate
relationship
between
and
phenotypic
age;
(iii)
explore
role
of
exercise
this
relationship.
Phenotypic
age
as
novel
index
was
calculated
according
biomarkers
collected
from
adults
based
on
National
Health
Nutrition
Examination
Survey
(NHANES).
information
self-reported
by
participants
discerned
through
individual
interviews.
The
principal
analytical
method
employed
weighted
multivariable
linear
regression
modeling,
which
accommodated
for
complex
multi-stage
sampling
design.
potential
non-linear
explored
using
restricted
cubic
spline
(RCS)
model.
Furthermore,
subgroup
analyses
evaluated
effects
sociodemographic
lifestyle
factors
primary
outcomes.
A
total
13,569
were
finally
included
in,
thereby
resulting
population
78,880,615.
An
examination
temporal
trends
revealed
declining
proportion
individuals
with
insufficient
markedly
deficient
time
since
2015-2016
cycle.
Taken
normal
group
reference,
extreme
short
[β
(95%
CI)
0.582
(0.018,
1.146),
p
=
0.044]
long
0.694
(0.186,
1.203),
0.010]
both
positively
associated
fully
adjusted
According
dose-response
age,
benefit
regular
activity,
whereas
more
tended
have
higher
age.
There
an
inverted
U-shaped
durations
represents
important
step
forward
our
understanding
By
shedding
light
topic
providing
practical
recommendations
habits,
researchers
help
live
longer,
healthier,
fulfilling
lives.
Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
134(14)
Published: July 14, 2024
A
growing
body
of
research
has
identified
circadian-rhythm
disruption
as
a
risk
factor
for
metabolic
health.
However,
the
underlying
biological
basis
remains
complex,
and
complete
molecular
mechanisms
are
unknown.
There
is
emerging
evidence
from
animal
human
to
suggest
that
expression
core
circadian
genes,
such
locomotor
output
cycles
kaput
gene
(CLOCK),
brain
muscle
ARNT-Like
1
(BMAL1),
period
(PER),
cyptochrome
(CRY),
consequent
hundreds
genes
integral
regulation
cellular
metabolism.
These
represent
potential
pathophysiological
pathways
linking
adverse
health
outcomes,
including
obesity,
syndrome,
type
2
diabetes.
Here,
we
aim
summarize
select
in
vivo
models
compare
these
results
with
epidemiologic
findings
advance
understanding
existing
foundational
mechanistic
links
between
altered
clock
contributions
health-related
pathologies.
Findings
have
important
implications
treatment,
prevention,
control
pathologies
leading
causes
death
disability,
diabetes,
cardiovascular
disease,
cancer.
Sleep
loss
can
severely
impair
the
ability
to
perform,
yet
recover
from
sleep
is
not
well
understood.
regulatory
processes
are
assumed
lie
exclusively
within
brain
mainly
due
strong
behavioral
manifestations
of
sleep.
Whole-body
knockout
circadian
clock
gene
Bmal1
in
mice
affects
several
aspects
sleep,
however,
cells/tissues
responsible
unknown.
We
found
that
restoring
expression
brains
Bmal1-knockout
did
rescue
Bmal1-dependent
phenotypes.
Surprisingly,
most
sleep-amount,
but
sleep-timing,
phenotypes
could
be
reproduced
or
rescued
by
knocking
out
BMAL1
skeletal
muscle,
respectively.
also
overexpression
skeletal-muscle
reduced
recovery
response
loss.
Together,
these
findings
demonstrate
muscle
both
necessary
and
sufficient
regulate
total
amount
reveal
critical
components
normal
regulation
occur
muscle.
SLEEP,
Journal Year:
2017,
Volume and Issue:
unknown
Published: July 22, 2017
The
metabolic
impact
of
inadequate
sleep
has
not
been
determined
in
healthy
individuals
outside
laboratories.
This
study
aims
to
investigate
the
duration
on
five
syndrome
components
a
adult
cohort.A
total
162121
adults
aged
20-80
years
(men
47.4%)
MJ
Health
Database,
who
were
obese
and
free
from
major
diseases,
recruited
followed
up
1996
2014.
Sleep
insomnia
symptoms
assessed
by
self-administered
questionnaire.
Incident
cases
identified
follow-up
medical
examinations.
Cox
proportional
hazard
ratios
(HRs)
calculated
for
three
categories
"<
6
hours/day
(short),"
"6-8
(regular),"
">
8
(long)"
with
adjustment
potential
confounding
factors.
Analyses
stratified
assess
whether
modified
association
between
syndrome.Compared
regular
duration,
short
significantly
(p
<
.001)
increased
risk
central
obesity
12%
(adjusted
HR
1.12
[1.07-1.17]),
elevated
fasting
glucose
6%
1.06
[1.03-1.09]),
high
blood
pressure
8%
1.08
[1.04-1.13]),
low
high-density
lipoprotein-cholesterol
7%
1.07
[1.03-1.11]),
hypertriglyceridemia
9%
1.09
[1.05-1.13]),
[1.05-1.13]).
Long
decreased
0.89
[0.84-0.94])
0.93
[0.88-0.99]).
Insomnia
did
modify
effects
duration.Sleep
may
be
significant
determinant
health.
Science Advances,
Journal Year:
2018,
Volume and Issue:
4(8)
Published: Aug. 3, 2018
Curtailed
sleep
promotes
weight
gain
and
loss
of
lean
mass
in
humans,
although
the
underlying
molecular
mechanisms
are
poorly
understood.
We
investigated
genomic
physiological
impact
acute
peripheral
tissues
by
obtaining
adipose
tissue
skeletal
muscle
after
one
night
full
sleep.
find
that
alters
genome-wide
DNA
methylation
tissue,
unbiased
transcriptome-,
protein-,
metabolite-level
analyses
also
reveal
highly
tissue-specific
changes
partially
reflected
altered
metabolite
levels
blood.
observe
transcriptomic
signatures
inflammation
both
following
loss,
but
involving
circadian
clock
evident
only
muscle,
we
uncover
suggestive
breakdown
contrast
with
an
anabolic
signature.
Our
findings
provide
insight
into
how
disruption
rhythms
may
promote
sarcopenia.
Frontiers in Neural Circuits,
Journal Year:
2018,
Volume and Issue:
12
Published: Feb. 26, 2018
Sleep
deprivation
disrupts
the
lives
of
millions
people
every
day
and
has
a
profound
impact
on
molecular
biology
brain.
These
effects
begin
as
changes
within
neuron,
at
DNA
RNA
level,
result
in
alterations
neuronal
plasticity
dysregulation
many
cognitive
functions
including
learning
memory.
The
epigenome
plays
critical
role
regulating
gene
expression
context
memory
storage.
In
this
review,
we
by
describing
epigenetic
regulation
expression,
focusing
most
common
mechanisms:
(i)
methylation,
(ii)
histone
modifications,
(iii)
non-coding
RNAs.
We
then
discuss
evidence
suggesting
that
sleep
loss
impacts
these
might
mediate
cognition
seen
following
disruption
sleep.
link
between
is
only
beginning
to
be
elucidated,
but
clear
exists
occur
deprivation.
future,
could
utilized
biomarkers
or
therapeutic
targets
for
sleep-related
disorders.
