Frontiers in Medicine,
Journal Year:
2021,
Volume and Issue:
8
Published: April 13, 2021
Obesity
is
one
of
the
epidemics
our
era.
Its
prevalence
higher
than
30%
in
U.S.
and
it
estimated
to
increase
by
50%
2030.
associated
with
a
risk
all-cause
mortality
known
be
cause
chronic
kidney
disease
(CKD).
Typically,
obesity-related
glomerulopathy
(ORG)
ascribed
renal
hemodynamic
changes
that
lead
hyperfiltration,
albuminuria
and,
finally,
impairment
glomerular
filtration
rate
due
glomerulosclerosis.
Though
not
only
hemodynamics
are
responsible
for
ORG:
adipokines
could
local
effects
on
mesangial
tubular
cells
podocytes
promoting
maladaptive
responses
hyperfiltration.
Furthermore,
hypertension
type
2
diabetes
mellitus,
two
conditions
generally
obesity,
both
amplifiers
obesity
injury
parenchyma,
as
well
complications
overweight.
As
native
kidney,
also
related
worse
outcomes
transplantation.
Despite
its
impact
CKD
cardiovascular
morbility
mortality,
therapeutic
strategies
fight
against
were
limited
decades
renin-angiotensin
blockade
bariatric
surgery
patients
who
accomplished
very
restrictive
criteria.
Last
years,
different
drugs
have
been
approved
or
under
study
treatment
obesity.
Glucagon-like
peptide-1
receptor
agonists
promising
since
they
shown
benefits
terms
losing
weight
obese
patients,
preventing
onset
macroalbuminuria
slowing
decline
eGFR
diabetes.
These
new
families
glucose-lowering
frontier
crossed
nephrologists
stop
progression.
Circulation Research,
Journal Year:
2020,
Volume and Issue:
126(6), P. 789 - 806
Published: March 12, 2020
Obesity
and
hypertension,
which
often
coexist,
are
major
risk
factors
for
heart
failure
characterized
by
chronic,
low-grade
inflammation,
promotes
adverse
cardiac
remodeling.
While
macrophages
play
a
key
role
in
remodeling,
dysregulation
of
macrophage
polarization
between
the
proinflammatory
M1
anti-inflammatory
M2
phenotypes
excessive
inflammation
injury.
Metabolic
shifting
glycolysis
mitochondrial
oxidative
phosphorylation
has
been
implicated
polarization.
primarily
rely
on
glycolysis,
whereas
tricarboxylic
acid
cycle
phosphorylation;
thus,
that
affect
metabolism
may
disrupt
M1/M2
homeostasis
exacerbate
inflammation.
The
mechanisms
obesity
hypertension
synergistically
induce
metabolic
dysfunction,
particularly
during
not
fully
understood.
We
propose
via
directly
target
metabolism,
including
changes
circulating
glucose
fatty
substrates,
lipotoxicity,
tissue
hypoxia.
discuss
canonical
novel
roles
obesity-hypertension-induced
injury,
diastolic
dysfunction
impaired
calcium
handling.
Finally,
we
current
status
potential
therapies
to
failure,
antidiabetic
therapies,
immunometabolic
agents.
Nutrients,
Journal Year:
2021,
Volume and Issue:
13(11), P. 4176 - 4176
Published: Nov. 22, 2021
Obesity
has
become
a
major
epidemic
in
the
21st
century.
It
increases
risk
of
dyslipidemia,
hypertension,
and
type
2
diabetes,
which
are
known
cardiometabolic
factors
components
metabolic
syndrome.
Although
overt
cardiovascular
(CV)
diseases
such
as
stroke
or
myocardial
infarction
domain
adulthood,
it
is
evident
that
CV
continuum
begins
very
early
life.
Recognition
stages
damage,
at
time
when
these
processes
still
reversible,
development
prevention
strategies
pillars
reducing
morbidity
mortality
general
population.
In
this
review,
we
will
discuss
role
well-known
but
also
novel
linking
obesity
increased
from
prenatal
age
to
including
perinatal
factors,
diet,
nutrigenomics,
nutri-epigenetics,
hyperuricemia,
cardiorespiratory
fitness.
The
importance
‘tracking’
on
adult
health
highlighted
economic
impact
childhood
well
preventive
discussed.
Hypertension,
Journal Year:
2021,
Volume and Issue:
78(5), P. 1197 - 1205
Published: Oct. 4, 2021
Epidemiological
studies
have
documented
that
insulin
resistance
and
diabetes
not
only
constitute
metabolic
abnormalities
but
also
predispose
to
hypertension,
vascular
stiffness,
associated
cardiovascular
disease.
Meanwhile,
excessive
arterial
stiffness
impaired
vasorelaxation,
in
turn,
contribute
worsening
the
development
of
diabetes.
Molecular
mechanisms
promoting
hypertension
include
inappropriate
activation
renin-angiotensin-aldosterone
system
sympathetic
nervous
system,
mitochondria
dysfunction,
oxidative
stress,
systemic
inflammation.
This
review
highlights
recent
which
uncovered
new
underlying
for
increased
propensity
association
with
These
enhanced
epithelial
sodium
channels,
alterations
extracellular
vesicles
their
microRNAs,
abnormal
gut
microbiota,
renal
sodium-glucose
cotransporter
activity,
collectively
covers
socioeconomic
factors
currently
recommended
blood
pressure
targets
related
treatment
strategies
diabetic
patients
hypertension.
Cardiovascular Research,
Journal Year:
2022,
Volume and Issue:
118(18), P. 3434 - 3450
Published: July 26, 2022
Abstract
Obesity
and
heart
failure
with
preserved
ejection
fraction
(HFpEF)
represent
two
intermingling
epidemics
driving
perhaps
the
greatest
unmet
health
problem
in
cardiovascular
medicine
21st
century.
Many
patients
HFpEF
are
either
overweight
or
obese,
recent
data
have
shown
that
increased
body
fat
its
attendant
metabolic
sequelae
widespread,
protean
effects
systemically
on
system
leading
to
symptomatic
HFpEF.
The
paucity
of
effective
therapies
underscores
importance
understanding
distinct
pathophysiological
mechanisms
obese
develop
novel
therapies.
In
this
review,
we
summarize
current
non-cardiovascular
features
phenotype
HFpEF,
how
adiposity
might
pathophysiologically
contribute
phenotype,
these
processes
be
targeted
therapeutically.
Cardiovascular Research,
Journal Year:
2020,
Volume and Issue:
117(8), P. 1859 - 1876
Published: Nov. 17, 2020
Abstract
Obesity
contributes
65–75%
of
the
risk
for
human
primary
(essential)
hypertension
(HT)
which
is
a
major
driver
cardiovascular
and
kidney
diseases.
Kidney
dysfunction,
associated
with
increased
renal
sodium
reabsorption
compensatory
glomerular
hyperfiltration,
plays
key
role
in
initiating
obesity-HT
target
organ
injury.
Mediators
dysfunction
blood
pressure
include
(i)
elevated
sympathetic
nerve
activity
(RSNA);
(ii)
antinatriuretic
hormones
such
as
angiotensin
II
aldosterone;
(iii)
relative
deficiency
natriuretic
hormones;
(iv)
compression
by
fat
around
kidneys;
(v)
activation
innate
adaptive
immune
cells
that
invade
tissues
throughout
body,
producing
inflammatory
cytokines/chemokines
contribute
to
vascular
injury,
exacerbate
HT.
These
neurohormonal,
renal,
mechanisms
are
interdependent.
For
example,
excess
adiposity
increases
adipocyte-derived
cytokine
leptin
RSNA
stimulating
central
nervous
system
proopiomelanocortin-melanocortin
4
receptor
pathway.
Excess
visceral,
perirenal
sinus
compress
kidneys
which,
along
RSNA,
renin–angiotensin–aldosterone
activation,
although
obesity
may
also
activate
mineralocorticoid
receptors
independent
aldosterone.
Prolonged
obesity,
HT,
metabolic
abnormalities,
inflammation
cause
progressive
making
HT
more
resistant
therapy
often
requiring
multiple
antihypertensive
drugs
concurrent
treatment
dyslipidaemia,
insulin
resistance,
diabetes,
inflammation.
More
effective
anti-obesity
needed
prevent
cascade
cardiorenal,
metabolic,
disorders
threaten
overwhelm
health
care
systems
prevalence
continues
increase.
Hypertension,
Journal Year:
2021,
Volume and Issue:
78(5)
Published: Sept. 20, 2021
Hypertension
is
a
major
risk
factor
for
cardiovascular
and
renal
diseases
in
the
United
States
worldwide.
Obesity
accounts
much
of
primary
hypertension
through
several
mechanisms,
including
neurohormonal
activation,
inflammation,
kidney
dysfunction.
As
prevalence
obesity
continues
to
increase,
associated
cardiorenal
will
also
increase
unless
more
effective
strategies
prevent
treat
are
developed.
Lifestyle
modification,
diet,
reduced
sedentariness,
increased
physical
activity,
usually
recommended
patients
with
obesity;
however,
long-term
success
these
reducing
adiposity,
maintaining
weight
loss,
blood
pressure
has
been
limited.
Effective
pharmacotherapeutic
procedural
strategies,
metabolic
surgeries,
additional
options
or
attenuate
hypertension,
target
organ
damage,
subsequent
disease.
Medications
can
be
useful
short-
treatment;
prescription
drugs
Metabolic
surgery
producing
sustained
loss
treating
disorders
many
severe
obesity.
Unanswered
questions
remain
related
mechanisms
obesity-related
diseases,
efficacy
different
treatment
prevention
timing
interventions
hypertension-mediated
damage.
Further
investigation,
randomized
controlled
trials,
essential
addressing
questions,
emphasis
should
placed
on
reduce
burden
hypertensive
mortality.