Nutrition & Metabolism,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Dec. 18, 2024
Sarcopenia,
characterized
by
progressive
and
generalized
loss
of
skeletal
muscle
(SkM)
mass,
strength,
physical
performance,
is
a
prevalent
complication
in
type
2
diabetes
(T2D).
Nitric
oxide
(NO),
multifunctional
gasotransmitter
involved
whole-body
glucose
insulin
homeostasis,
plays
key
roles
normal
SkM
physiology
function.
Here,
we
highlight
the
role
NO
mass
maintenance
its
potential
contribution
to
development
T2D-related
sarcopenia.
Physiologic
level,
primarily
produced
sarcolemmal
neuronal
nitric
synthase
(nNOSμ
isoform),
protein
synthesis
fibers
mass.
The
observed
effect
nNOSμ
on
muscle-type
specific
sex-dependent.
Impaired
homeostasis
[due
diminished
nNOSμ-NO
availability
excessive
production
through
inducible
NOS
(iNOS)
response
atrophic
stimuli,
e.g.,
inflammatory
cytokines]
occurred
during
progression
T2D,
may
cause
Theoretically,
restoration
nNOS
overexpression,
supplying
substrates
(e.g.,
L-arginine
L-citrulline),
phosphodiesterase
(PDE)
inhibition,
supplementation
with
donors
inorganic
nitrate)
be
therapeutic
approaches
preserve
prevents
sarcopenia
T2D.
Journal of Diabetes,
Journal Year:
2024,
Volume and Issue:
16(10)
Published: Oct. 1, 2024
Abstract
Type
2
diabetes
mellitus
(T2DM)
is
a
chronic
metabolic
disorder
with
the
increasing
prevalence
of
modern
sedentary
lifestyle.
Wearable
technology‐based
physical
activity
interventions
(WT‐BPAI)
might
provide
channel
to
improve
diabetic
self‐management.
The
study
aimed
(1)
evaluate
effectiveness
WT‐BPAI
on
PA
levels,
glycemic
and
other
outcomes
(blood
pressure
[BP],
body
mass
index
[BMI],
serum
lipid
profile)
in
adults
T2DM,
(2)
investigate
potential
covariates
affecting
aforementioned
outcomes.
Eight
databases
were
searched
thoroughly
using
three
steps
from
inception
until
January
16,
2024.
quality
studies
overall
evidence
evaluated.
package
meta
R
software
program
version
4.3.1.
was
utilized
for
meta‐analyses,
subgroup
analyses,
meta‐regression
analyses.
A
total
19
randomized
controlled
trials
(RCTs)
found.
Meta‐analyses
revealed
that
significantly
increased
1583
per
day
decreased
systolic
BP
(SBP)
by
2.46
mmHg.
Subgroup
analyses
found
function,
duration
intervention,
age
significant
covariates.
According
risk
bias
2,
more
than
half
raised
some
concerns
about
randomization
process,
deviations
intended
missing
outcome
data.
certainty
very
low
all
based
Grading
Recommendations
Assessment,
Development
Evaluation
(GRADE)
criteria.
can
be
considered
supplementary
intervention
increase
decrease
SBP,
especially
when
used
short
periods
young
T2DM.
However,
we
need
well‐designed
research
long‐term
image
Photobiomodulation Photomedicine and Laser Surgery,
Journal Year:
2024,
Volume and Issue:
42(12), P. 768 - 778
Published: Oct. 23, 2024
Heart
failure
(HF)
and
type
2
diabetes
mellitus
(DM2)
are
global
health
problems
that
often
lead
to
muscle
atrophy.
These
conditions
associated
with
increased
autophagy
apoptosis
in
the
cells,
resulting
decreased
mass.
Physical
exercise
photobiomodulation
(PBM)
seems
promising
attenuate
skeletal
changes
caused
by
HF
DM2,
due
its
direct
effects
on
mitochondria,
which
may
result
an
increase
antioxidant
capacity.
The journal of nutrition health & aging,
Journal Year:
2024,
Volume and Issue:
28(6), P. 100229 - 100229
Published: April 9, 2024
Supplementation
with
β-hydroxy
β-methyl
butyrate
(HMB)
appears
to
be
effective
in
preserving
muscle
older
adults.
However,
the
association
between
endogenously
produced
HMB
frailty
has
not
been
studied
people
chronic
disease.
The
purpose
of
this
study
is
explore
whether
an
exists
endogenous
levels
and
status
adults
type-2
diabetes
mellitus
(T2DM).
Data
were
taken
from
Toledo
Study
Healthy
Ageing,
a
community-dwelling
aged
(65
years+)
cohort.
Frailty
was
assessed
at
baseline
2.99
median
years
according
Phenotype
(FP)
standardized
our
population
Trait
Scale
12
(FTS12).
associations
using
three
nested
multivariate
logistic
regressions
segmented
by
sex.
Glucose,
glucose
interaction,
age
body
composition
used
as
covariables.
255
participants
(mean
75.3
years,
52.94%
men)
included.
showed
inverse
cross-sectional
frailty,
which
modified
when
interaction
term
HMB*glucose
included,
remaining
significant
only
for
FTS12
[OR
(95%
CI):
0.436
(0.253,
0.751),
p-value
0.003].
independent
sex,
maintained
after
adjusting
covariates.
there
threshold
points
levels,
above
protective
effect
lost:
145.4
mg/dl
adjusted
gender
whole
sample
149.6
138.9
men
women,
respectively.
Endogenous
found
associated
incident
frailty.
Cross-sectional
analysis
revealed
that
inversely
T2DM.
This
dependent
on
circulating
fasted
levels.
Meditsinskiy sovet = Medical Council,
Journal Year:
2024,
Volume and Issue:
6, P. 16 - 22
Published: May 8, 2024
The
prevalence
of
type
2
diabetes
among
older
people
is
increasing
every
year.
main
pathogenetic
mechanisms
in
elderly
patients
include
disruption
the
intestinal
microbiota,
cellular
aging,
oxidative
stress
and
mitochondrial
dysfunction,
immune
inflammatory
processes.
Short-chain
fatty
acids
produced
by
microbiota
influence
processes
pancreatic
β-cells.
Cellular
senescence
causes
secretion
different
cytokines,
chemokines,
growth
factors
proteases,
exacerbating
proinflammatory
state
insulin
resistance
tissues.
Oxidative
dysfunction
decrease
ATP
synthesis
process
increase
formation
reactive
oxygen
species.
Changes
system
contribute
to
autoimmune
systemic
inflammation.
Clinical
features
mellitus
old
age
asymptomatic
progression,
impaired
recognition
hypoglycemia,
cognitive
function,
muscle
atrophy.
progressive
decline
β-cells
function
requires
therapy
many
patients.
Biphasic
insulins
allow
control
both
basal
postprandial
glycemia,
are
easy
use
indicated
for
who
have
difficulty
counting
amount
carbohydrates.
However,
it
worth
remembering
a
balanced
approach
prescribing
deintensifying
therapy.
Life,
Journal Year:
2024,
Volume and Issue:
14(7), P. 784 - 784
Published: June 21, 2024
Type
2
diabetes
mellitus
(T2DM)
is
a
burgeoning
public
health
challenge
worldwide.
Individuals
with
T2DM
are
at
increased
risk
for
skeletal
muscle
atrophy,
serious
complication
that
significantly
compromises
quality
of
life
and
which
effective
prevention
measures
currently
inadequate.
Emerging
evidence
indicates
systemic
local
inflammation
stemming
from
the
compromised
intestinal
barrier
one
crucial
mechanisms
contributing
to
atrophy
in
patients.
Notably,
natural
plant
polysaccharides
were
found
be
capable
enhancing
function
mitigating
secondary
some
diseases.
Herein,
we
hypothesized
Clinical Case Reports,
Journal Year:
2024,
Volume and Issue:
12(11)
Published: Oct. 30, 2024
Key
Clinical
Message
External
muscle
stimulation,
possibly
combined
with
active
contraction,
could
improve
physical
functioning
and
performance
in
inclusion
body
myositis.
Abstract
Inclusion
myositis
(IBM)
is
a
chronic,
progressive
inflammatory
disease
largely
unknown
causes.
It
typically
affects
men
more
than
women,
usually
beginning
the
latter
half
of
life.
IBM
leads
to
weakness
wasting,
especially
arms
legs,
which
significantly
impairs
daily
complicates
participation
exercise
training.
Few
studies
have
examined
impact
training
on
fitness,
inflammation
markers,
quality
life
patients.
The
patient,
Caucasian
male
(78.3
kg,
174.0
cm,
born
October
1948),
was
diagnosed
2011.
From
2017
September
2019,
he
underwent
focused
external
stimulation
contractions.
Regular
assessments
included
cardiopulmonary
testing,
functional
tests
(6‐min
walking
test,
modified
timed
up
go
chair
rise
test),
lung
function
exams,
blood
parameters,
composition,
questionnaires.
decline
fitness
may
been
slowed
during
intervention
period,
as
indicated
by
some
improvements
like
peak
oxygen
uptake
test
results
while
other
parameters
remained
unchanged
or
declined
power
output,
fat‐free
mass
functioning.
However,
recurrence
his
prostate
cancer
after
treatment
androgen
deprivation
therapy
led
further
declines
thus
increased
wasting.
data
suggest
that
supportive
programs
focusing
might
functioning,
performance,
management.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: Nov. 5, 2024
Diabetes
is
one
of
the
most
common
metabolic
diseases
worldwide,
leading
to
complications,
mortality,
and
significant
healthcare
expenditures,
which
impose
a
substantial
social
financial
burden
globally.
A
diabetic
environment
can
induce
changes,
negatively
affecting
tendon
homeostasis,
alterations
in
biomechanical
properties
histopathology.
Numerous
studies
have
investigated
mechanisms
through
diabetes
exerts
pathological
effects
on
tendons,
including
increased
free
radical
production,
oxidative
stress,
inflammatory
responses,
deposition
advanced
glycation
end
products
(AGEs),
microvascular
changes.
These
changes
damages
structure,
biomechanics,
repair
processes.
The
proliferation
stem
cells
decreases,
apoptosis
increases,
abnormal
differentiation,
along
with
expression
myofibroblasts,
ultimately
lead
insufficient
repair,
fibrosis,
remodeling.
Although
researches
unveiling
tendinopathy,
fibrosis
or
contracture,
injury
healing
are
growing,
systematic
understanding
still
lacking.
Therefore,
this
review
summarizes
current
research
status
provides
comprehensive
overview,
offering
theoretical
guidance
for
future
in-depth
exploration
impact
tendons
development
treatments
diabetes-related
diseases.
Nutrition & Metabolism,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Dec. 18, 2024
Sarcopenia,
characterized
by
progressive
and
generalized
loss
of
skeletal
muscle
(SkM)
mass,
strength,
physical
performance,
is
a
prevalent
complication
in
type
2
diabetes
(T2D).
Nitric
oxide
(NO),
multifunctional
gasotransmitter
involved
whole-body
glucose
insulin
homeostasis,
plays
key
roles
normal
SkM
physiology
function.
Here,
we
highlight
the
role
NO
mass
maintenance
its
potential
contribution
to
development
T2D-related
sarcopenia.
Physiologic
level,
primarily
produced
sarcolemmal
neuronal
nitric
synthase
(nNOSμ
isoform),
protein
synthesis
fibers
mass.
The
observed
effect
nNOSμ
on
muscle-type
specific
sex-dependent.
Impaired
homeostasis
[due
diminished
nNOSμ-NO
availability
excessive
production
through
inducible
NOS
(iNOS)
response
atrophic
stimuli,
e.g.,
inflammatory
cytokines]
occurred
during
progression
T2D,
may
cause
Theoretically,
restoration
nNOS
overexpression,
supplying
substrates
(e.g.,
L-arginine
L-citrulline),
phosphodiesterase
(PDE)
inhibition,
supplementation
with
donors
inorganic
nitrate)
be
therapeutic
approaches
preserve
prevents
sarcopenia
T2D.
