International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(13), P. 3299 - 3299
Published: July 5, 2019
The
term
diabetic
cardiomyopathy
(DCM)
labels
an
abnormal
cardiac
structure
and
performance
due
to
intrinsic
heart
muscle
malfunction,
independently
of
other
vascular
co-morbidity.
DCM,
accounting
for
50%-80%
deaths
in
patients,
represents
a
worldwide
problem
human
health
related
economics.
Optimal
glycemic
control
is
not
sufficient
prevent
which
derives
from
remodeling
geometrical
changes,
with
both
consequences
critical
events
initially
occurring
at
the
cardiomyocyte
level.
Cardiac
cells,
under
hyperglycemia,
very
early
undergo
metabolic
abnormalities
contribute
T
helper
(Th)-driven
inflammatory
perturbation,
behaving
as
immunoactive
units
capable
releasing
biomediators,
such
cytokines
chemokines.
This
paper
aims
focus
onto
role
cardiomyocytes,
no
longer
considered
"passive"
targets
but
"active"
participating
dialogue
between
local
systemic
counterparts
underlying
DCM
development
maintenance.
Some
main
biomolecular/metabolic/inflammatory
processes
triggered
within
cells
by
high
glucose
are
overviewed;
particular
attention
addressed
chemokines,
representing
potential
therapeutic
prompt
intervention
when
signs
or
symptoms
manifesting
yet.
clinical
management
still
challenge
further
translational
investigations,
including
studies
female/male
cell
level,
warranted.
Diabetes/Metabolism Research and Reviews,
Journal Year:
2020,
Volume and Issue:
37(2)
Published: June 27, 2020
The
outbreak
of
the
coronavirus
disease
2019
(Covid-19)
has
become
an
evolving
worldwide
health
crisis.
With
rising
prevalence
obesity
and
diabetes
come
increasing
awareness
their
impacts
on
infectious
diseases,
including
increased
risk
for
various
infections,
post-infection
complications
mortality
from
critical
infections.
Although
epidemiological
clinical
characteristics
Covid-19
have
been
constantly
reported,
no
article
systematically
illustrated
role
in
Covid-19,
or
how
affects
diabetes,
special
treatment
these
at-risk
populations.
Here,
we
present
a
synthesis
recent
advances
our
understanding
relationships
between
obesity,
along
with
underlying
mechanisms,
provide
guidance
Journal of Clinical Investigation,
Journal Year:
2017,
Volume and Issue:
127(1), P. 5 - 13
Published: Jan. 2, 2017
Chronic
inflammation
in
adipose
tissue,
possibly
related
to
cell
hypertrophy,
hypoxia,
and/or
intestinal
leakage
of
bacteria
and
their
metabolic
products,
likely
plays
a
critical
role
the
development
obesity-associated
insulin
resistance
(IR).
Cells
both
innate
adaptive
immune
system
residing
tissues,
as
well
intestine,
participate
this
process.
Thus,
M1
macrophages,
IFN-γ-secreting
Th1
cells,
CD8+
T
B
cells
promote
IR,
part
through
secretion
proinflammatory
cytokines.
Conversely,
eosinophils,
Th2
type
2
lymphoid
Foxp3+
Tregs
protect
against
IR
local
control
inflammation.
Journal of Leukocyte Biology,
Journal Year:
2018,
Volume and Issue:
104(3), P. 525 - 534
Published: Aug. 1, 2018
Abstract
Obesity
and
type
2
diabetes
mellitus
(T2D)
are
global
pandemics.
Worldwide,
the
prevalence
of
obesity
has
nearly
tripled
since
1975
T2D
almost
doubled
1980.
Both
indolent
chronic
diseases
that
develop
gradually,
with
cellular
physiologic
changes
occurring
before
clinical
signs
symptoms
become
apparent.
Individuals
physiologically
frail
have
an
increased
risk
infections
mortality
from
sepsis.
Improvement
in
morbidity
these
at-risk
populations
would
provide
a
great
societal
benefit.
We
believe
worsened
outcomes
observed
patient
is
due
to
immune
system
dysfunction
triggered
by
low-grade
inflammation
present
both
diseases.
As
modulatory
therapies
been
utilized
other
inflammatory
diseases,
there
emerging
role
for
target
chronically
affected
pathways
obese
patients.
Additionally,
bariatric
surgery
currently
most
successful
treatment
only
weight
loss
method
also
causes
sustained,
substantial
improvement
T2D.
Consequently,
may
improving
immunity
populations.
Review
on
how
impact
lead
poor
after
loss.
AJP Renal Physiology,
Journal Year:
2016,
Volume and Issue:
312(4), P. F716 - F731
Published: Aug. 25, 2016
Increasing
incidences
of
obesity
and
diabetes
have
made
diabetic
kidney
disease
(DKD)
the
leading
cause
chronic
end-stage
renal
worldwide.
Despite
current
pharmacological
treatments,
including
strategies
for
optimizing
glycemic
control
inhibitors
renin-angiotensin
system,
DKD
still
makes
up
almost
one-half
all
cases
in
United
States.
Compelling
mounting
evidence
has
clearly
demonstrated
that
immunity
inflammation
play
a
paramount
role
pathogenesis
DKD.
This
article
reviews
involvement
immune
system
identifies
important
roles
key
inflammatory
mediators.
One
most
recently
identified
biomarkers
is
serum
amyloid
A,
which
appears
to
be
relatively
specific
Novel
evolving
treatment
approaches
target
protein
kinases,
transcription
factors,
chemokines,
adhesion
molecules,
growth
advanced
glycation
end-products,
other
molecules.
beginning
new
era
understanding
DKD,
we
may
finally
reached
tipping
point
our
fight
against
growing
burden
Journal of Diabetes Research,
Journal Year:
2017,
Volume and Issue:
2017, P. 1 - 6
Published: Jan. 1, 2017
Although
a
critical
role
of
adaptive
immune
system
has
been
confirmed
in
driving
local
and
systemic
inflammation
type
2
diabetes
promoting
insulin
resistance,
the
underlying
mechanism
is
not
completely
understood.
Inflammatory
regulation
focused
on
innate
immunity
especially
macrophage
for
long
time,
while
increasing
evidence
suggests
T
cells
are
crucial
development
metabolic
resistance
since
2009.
There
was
growing
supporting
implication
pathogenesis
diabetes.
We
will
discuss
available
effect
subsets
associated
with
procession
T2DM,
which
may
unveil
several
potential
strategies
that
could
provide
successful
therapies
future.
Frontiers in Immunology,
Journal Year:
2019,
Volume and Issue:
10
Published: Feb. 5, 2019
Non-alcoholic
fatty
liver
disease
(NAFLD)
constitutes
a
spectrum
of
states
characterized
by
hepatic
steatosis
and
is
closely
associated
to
obesity
the
metabolic
syndrome.
In
non-alcoholic
steatohepatitis
(NASH),
additionally,
inflammatory
changes
hepatocellular
damage
are
present,
representing
more
severe
condition,
for
which
treatment
an
unmet
medical
need.
Pathophysiologically,
immune
system
one
main
drivers
NAFLD
progression
other
obesity-related
comorbidities,
both
innate
adaptive
involved.
T
cells
form
cellular
component
consist
multiple
differentially
active
subsets,
i.e.,
helper
(Th)
cells,
regulatory
(Treg)
cytotoxic
(Tc)
as
well
several
T-cell
subsets.
This
review
focuses
on
role
these
subsets
in
pathogenesis
NAFLD,
association
with
type
2
diabetes
mellitus,
reviewing
available
evidence
from
animal
human
studies.
Briefly,
Th1,
Th2,
Th17,
Th22
seem
have
attenuating
effect
adiposity.
Th22,
Treg
decrease
insulin
resistance,
whereas
Tc
aggravating
effect.
Concerning
appear
overall
tempering
effect,
Th17
induce
fibrosis
progression.
The
regarding
controversial
warrants
further
exploration.
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: July 12, 2021
Chronic
inflammation
plays
an
important
role
in
the
development
of
metabolic
diseases.
These
include
obesity,
type
2
diabetes
mellitus,
and
dysfunction-associated
fatty
liver
disease.
The
proinflammatory
environment
maintained
by
innate
immunity,
including
macrophages
related
cytokines,
can
be
influenced
adaptive
immunity.
function
T
helper
17
(Th17)
regulatory
(Treg)
cells
this
process
has
attracted
attention.
Th17/Treg
balance
is
regulated
inflammatory
cytokines
various
factors,
those
associated
with
cellular
energy
metabolism.
possible
underlying
mechanisms
metabolism-related
signaling
pathways
epigenetic
regulation.
Several
studies
conducted
on
human
animal
models
have
shown
marked
differences
roles
chronic
obesity
Moreover,
seems
to
a
bridge
linking
gut
microbiota
host
disorders.
In
review,
we
provided
overview
alterations
functions
diseases
its
regulating
immune
response-related
glucose
lipid
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
11
Published: Feb. 3, 2021
When
viruses
infect
cells,
they
almost
invariably
cause
metabolic
changes
in
the
infected
cell
as
well
several
host
types
that
react
to
infection.
Such
provide
potential
targets
for
therapeutic
approaches
could
reduce
impact
of
Several
examples
are
discussed
this
review,
which
include
effects
on
energy
metabolism,
glutaminolysis
and
fatty
acid
metabolism.
The
response
immune
system
also
involves
manipulating
these
may
change
outcome
This
changing
status
herpesviruses
infections
from
productive
latency.
consequences
viral
coronavirus
disease
2019
(COVID-19),
differ
patients
with
problems,
such
diabetes
mellitus
(DM),
obesity,
endocrine
diseases.
Nutrition
affect
pattern
events
following
infection
human
experimental
animal
diseases
mechanisms
involved
discussed.
Finally,
we
discuss
so
far
few
published
reports
have
manipulated
in-vivo
virus
topic
is
expected
expand
relevance
an
approach
used
alone
or
combination
other
therapies
shape
nature
induced
