Environmental
and
lifestyle
changes,
in
addition
to
the
ageing
of
populations,
are
generally
believed
account
for
rapid
global
increase
type
2
diabetes
prevalence
incidence
recent
decades.
In
this
review,
we
present
a
comprehensive
overview
factors
contributing
risk,
including
aspects
diet
quality
quantity,
little
physical
activity,
increased
monitor
viewing
time
or
sitting
general,
exposure
noise
fine
dust,
short
disturbed
sleep,
smoking,
stress
depression,
low
socioeconomic
status.
these
promote
an
body
mass
index.
Since
loss
β-cell
function
is
ultimate
cause
developing
overt
diabetes,
environmental
changes
must
have
resulted
higher
risk
damage
those
at
genetic
risk.
Multiple
mechanistic
pathways
may
come
into
play.
Strategies
prevention
should
aim
promoting
'diabetes-protective
lifestyle'
whilst
simultaneously
enhancing
resistance
human
organism
pro-diabetic
factors.
More
research
on
diabetes-protective
mechanisms
seems
warranted.
Obesity Reviews,
Год журнала:
2015,
Номер
17(4), С. 297 - 312
Опубликована: Дек. 29, 2015
Summary
The
composition
of
the
gut
microbiota
and
excessive
ingestion
high‐fat
diets
(HFD)
are
considered
to
be
important
factors
for
development
obesity.
In
this
review
we
describe
a
coherent
mechanism
action
obesity,
which
involves
microbiota,
HFD,
low‐grade
inflammation,
expression
fat
translocase
scavenger
receptor
CD36,
class
B
type
1
(SR‐BI).
SR‐BI
binds
both
lipids
lipopolysaccharide
(LPS)
from
Gram‐negative
bacteria,
may
promote
incorporation
LPS
in
chylomicrons
(CMs).
These
CMs
transported
via
lymph
circulation,
where
is
transferred
other
lipoproteins
by
translocases,
preferentially
HDL.
increases
binding,
transcytosis
over
endothelial
barrier,and
endocytosis
adipocytes.
Especially
large
size
adipocytes
with
high
metabolic
activity
absorb
LPS‐rich
lipoproteins.
addition,
macrophages
adipose
tissue
internalize
LPS‐lipoproteins.
This
contribute
polarization
M2
M1
phenotype,
consequence
increased
delivery
into
during
hypertrophy.
conclusion,
evidence
suggests
that
involved
obesity
as
direct
targeting
molecule
lipid
storage
tissue.
Frontiers in Immunology,
Год журнала:
2020,
Номер
11
Опубликована: Фев. 18, 2020
C-type
lectin-like
receptors
(CLRs)
represent
a
family
of
transmembrane
pattern
recognition
receptors,
expressed
primarily
by
myeloid
cells.
They
recognize
not
only
pathogen
moieties
for
host
defense,
but
also
modified
self-antigens
such
as
damage-associated
molecular
patterns
released
from
dead
Upon
ligation,
CLR
signaling
leads
to
the
production
inflammatory
mediators
shape
amplitude,
duration
and
outcome
immune
response.
Thus,
following
excessive
injury,
dysregulation
these
development
diseases.
Herein,
we
will
focus
on
four
CLRs
"Dectin
family",
shown
decode
immunogenicity
cell
death.
CLEC9A
dendritic
cells
links
F-actin
exposed
dying
favor
cross-presentation
dead-cell
associated
antigens
CD8+
T
Nevertheless,
exerts
feedback
mechanisms
temper
neutrophil
recruitment
prevent
additional
tissue
damage.
MINCLE
macrophages
binds
nuclear
SAP130
necrotic
potentiate
pro-inflammatory
responses.
However,
consequent
inflammation
can
exacerbate
pathogenesis
Moreover,
in
tumor
microenvironment,
induces
macrophage-induced
suppression
cancer
progression.
Similarly,
triggering
LOX-1
oxidized
LDL,
amplifies
response
promotes
escape
metastasis.
Finally,
CLEC12A
that
recognizes
monosodium
urate
crystals
formed
during
death,
inhibits
activating
signals
detrimental
inflammation.
Interestingly,
sustains
type-I
IFN
finely
tune
responses
case
viral-induced
collateral
Therefore,
acting
concert
sensors
could
be
used
targeted
way
treat
numerous
diseases
allergies,
obesity,
tumors
autoimmunity.
Lifestyle
factors
conferring
increased
diabetes
risk
are
associated
with
elevated
basal
insulin
levels
(hyperinsulinaemia).
The
latter
predicts
later
obesity
in
children
and
adolescents.
A
causal
role
of
hyperinsulinaemia
for
adipose
tissue
growth
is
probable
because
pharmacological
reduction
secretion
lowers
body
weight
people
who
obese.
Genetic
inactivation
gene
alleles
mice
also
their
systemic
prevents
or
ameliorates
high-fat
diet-induced
obesity.
Hyperinsulinaemia
causes
gain
a
physiological
property
insulin.
Insulin
that
on
the
high
side
normal,
which
slightly
elevated,
sufficient
to
suppress
lipolysis
promote
lipogenesis
adipocytes.
effect
glucose
transport
hepatic
production
requires
six
two
times
higher
hormone
levels,
respectively.
It
seems
justified
suggest
lifestyle
avoids
order
limit
anabolic
fat
activity.
Frontiers in Molecular Biosciences,
Год журнала:
2022,
Номер
9
Опубликована: Май 25, 2022
Cardiovascular
disease
(CVD)
is
still
the
leading
cause
of
death
globally,
and
atherosclerosis
main
pathological
basis
CVDs.
Low-density
lipoprotein
cholesterol
(LDL-C)
a
strong
causal
factor
atherosclerosis.
However,
first-line
lipid-lowering
drugs,
statins,
only
reduce
approximately
30%
CVD
risk.
Of
note,
atherosclerotic
(ASCVD)
cannot
be
eliminated
in
great
number
patients
even
their
LDL-C
levels
meet
recommended
clinical
goals.
Previously,
whether
elevated
plasma
level
triglyceride
causally
associated
with
ASCVD
has
been
controversial.
Recent
genetic
epidemiological
studies
have
demonstrated
that
triglyceride-rich
(TGRL)
are
risk
factors
residual
ASCVD.
TGRLs
metabolites
can
promote
via
modulating
inflammation,
oxidative
stress,
formation
foam
cells.
In
this
article,
we
will
make
short
review
TG
TGRL
metabolism,
display
evidence
association
between
ASCVD,
summarize
atherogenic
metabolites,
discuss
current
findings
advances
TG-lowering
therapies.
This
provides
information
useful
for
researchers
field
as
well
pharmacologists
clinicians.
Diabetes & Metabolism Journal,
Год журнала:
2023,
Номер
47(5), С. 612 - 629
Опубликована: Сен. 26, 2023
Dyslipidemia
is
a
potentially
modifiable
cardiovascular
risk
factor.
Whereas
the
recommendations
for
treatment
target
of
dyslipidemia
in
general
population
are
being
more
and
rigorous,
2013
Kidney
Disease:
Improving
Global
Outcomes
clinical
practice
guideline
lipid
management
chronic
kidney
disease
(CKD)
presented
relatively
conservative
approach
with
respect
to
indication
lowering
therapy
therapeutic
monitoring
among
patients
CKD.
This
may
be
largely
attributed
lack
high-quality
evidence
derived
from
CKD
population,
whom
overall
feature
considerably
distinctive
that
population.
In
this
review
article,
we
cover
characteristic
features
impact
on
outcomes
We
also
current
modify
events
finally
discuss
association
between
progression
potential
strategy
delay
relation
therapy.
IL-1β
is
a
well-established
inducer
of
both
insulin
resistance
and
impaired
pancreatic
islet
function.
Despite
this,
findings
examining
IL-1
receptor
deficiency
or
antagonism
in
vivo
animal
models,
as
well
clinical
studies
type
2
diabetic
(T2D)
patients,
have
led
to
conflicting
results,
suggesting
that
the
actions
on
glycemic
control
may
be
pleiotropic
nature.
In
present
work,
we
find
ability
amplify
glucose-stimulated
secretion
from
human
islets
correlates
with
donor
BMI.
Islets
obese
donors
are
sensitized
insulinotropic
effects
this
cytokine,
whereas
stimulatory
lost
T2D
role
for
signaling
compensation.
Indeed,
mice
deficient
I
become
glucose
intolerant
more
rapidly
than
their
WT
littermates
secretory
responses
during
acute
stages
inflammatory
metabolic
stress
induced
by
LPS
high-fat
diet,
respectively.
directly
enhances
β
cell
increasing
granule
docking
soluble
N-ethylmaleimide-sensitive
factor
attachment
(SNARE)
complex
formation
at
plasma
membrane.
Together,
our
study
highlights
importance
compensation
stress.
American Journal of Clinical Nutrition,
Год журнала:
2021,
Номер
114(3), С. 1028 - 1038
Опубликована: Апрель 1, 2021
Meal-induced
metabolic
changes
trigger
an
acute
inflammatory
response,
contributing
to
chronic
inflammation
and
associated
diseases.
We
aimed
characterize
variability
in
postprandial
responses
using
traditional
(IL-6)
novel
[glycoprotein
acetylation
(GlycA)]
biomarkers
of
dissect
their
biological
determinants
with
a
focus
on
glycemia
lipemia.
Postprandial
(0–6
h)
glucose,
triglyceride
(TG),
IL-6,
GlycA
were
measured
at
multiple
intervals
after
sequential
mixed-nutrient
meals
(0
h
4
1002
healthy
adults
aged
18–65
y
from
the
PREDICT
(Personalised
REsponses
DIetary
Composition
Trial)
1
study,
single-arm
dietary
intervention
study.
Measures
habitual
diet,
blood
biochemistry,
gut
microbiome
composition,
visceral
fat
mass
(VFM)
also
collected.
The
IL-6
concentrations
highly
variable
between
individuals.
Participants
eliciting
increase
(60%
94%
total
participants,
respectively)
had
mean
6-h
increases
11%
190%,
respectively.
Peak
TG
glucose
significantly
(r
=
0.83
r
0.24,
respectively;
both
P
<
0.001)
but
not
(both
>
0.26).
A
random
forest
model
revealed
maximum
concentration
was
strongest
predictor
structural
equation
modeling
that
VFM
fasting
most
strongly
GlycA.
Network
Mendelian
randomization
demonstrated
causal
link
GlycA,
mediated
(28%)
by
TG.
Individuals
enhanced
higher
predicted
cardiovascular
disease
risk
(using
atherosclerotic
score)
than
rest
cohort.
associations
metabolism
highlight
importance
modulating
concert
obesity
reduce
low-grade
inflammation–related
This
trial
registered
clinicaltrials.gov
as
NCT03479866.
