Bone,
Journal Year:
2019,
Volume and Issue:
131, P. 115160 - 115160
Published: Nov. 20, 2019
Studies
have
shown
that
osteoporosis
and
atherosclerosis
are
comorbid
conditions
sharing
common
risk
factors
pathophysiological
mechanisms.
Understanding
these
is
crucial
in
order
to
develop
shared
methods
for
stratification,
prevention,
diagnosis
treatment.
The
aim
of
this
study
was
apply
a
system-level
bioinformatics
approach
lipidome-wide
data
pinpoint
the
lipidomic
architecture
jointly
associated
with
surrogate
markers
complex
diseases.
based
on
Cardiovascular
Risk
Young
Finns
Study
cohort
from
2007
follow-up
(n
=
1494,
aged
30–45
years,
women:
57%).
Liquid
chromatography-tandem
mass
spectrometry
(LC-MS/MS)
used
analyse
serum
lipidome,
involving
437
molecular
lipid
species.
subclinical
osteoporotic
included
indices
bone
mineral
density
content,
measured
using
peripheral
quantitative
computer
tomography
distal
shaft
sites
both
tibia
radius.
atherosclerotic
carotid
bulbus
intima
media
thickness
high-resolution
ultrasound.
Weighted
co-expression
network
analysis
performed
identify
networks
densely
interconnected
species
(i.e.
modules)
atherosclerosis.
levels
(lipid
profiles)
each
modules
were
summarized
by
first
principal
component
termed
as
module
eigenlipid.
Then,
Pearson's
correlation
(r)
calculated
between
eigenlipids
markers.
Lipid
significantly
correlated
considered
be
related
comorbidities.
hypothesis
profiles
constituent
joint
effects
tested
multivariate
variance
(MANOVA).
Among
twelve
studied
modules,
we
identified
one
105
(r
0.24,
p-value
2
×
10−20)
0.16,
10−10).
majority
belonged
glycerolipid
60),
glycerophospholipid
13)
sphingolipid
29)
classes.
also
enriched
ceramides
20),
confirming
their
significance
cardiovascular
outcomes
suggesting
role
top
three
37
statistically
significant
(adjusted
<
0.05)
within
all
triacylglycerols
(TAGs)
–
TAG(18:0/18:0/18:1)
an
adjusted
8.6
10−8,
TAG(18:0/18:1/18:1)
3.7
10−6,
TAG(16:0/18:0/18:1)
8.5
10−6.
This
novel
Alterations
metabolism
and,
more
specifically,
TAG
lipids
may
provide
potential
new
biomarkers
testing
comorbidities,
opening
avenues
emergence
dual-purpose
prevention
measures.
Biological and Pharmaceutical Bulletin,
Journal Year:
2015,
Volume and Issue:
39(1), P. 1 - 24
Published: Dec. 31, 2015
Increased
levels
of
apolipoprotein
B
(apoB)-containing
lipoproteins,
such
as
low
density
lipoproteins
(LDL)
and
chylomicron
remnants,
are
associated
with
the
development
atherosclerosis.
Chylomicrons
containing
apoB-48
secreted
from
intestine
during
postprandial
state,
whereas
very
(VLDL)
apoB-100
constitutively
formed
in
liver.
Chylomicron
remnants
VLDL
produced
by
lipoprotein
lipase-mediated
lipolysis
triglycerides,
which
is
activated
C-II
bound
on
particle
surfaces.
The
hepatic
uptake
these
facilitated
E
(apoE),
but
inhibited
apolipoproteins
C-I,
C-III.
In
plasma,
further
converted
into
LDL
hydrolysis
triglycerides.
ApoB-100
responsible
for
LDL.
receptor,
receptor-related
protein
heparan
sulfate
proteoglycans
involved
clearance
and/or
apoE.
subendothelial
retention
modification
apoB-containing
crucial
events
initiation
subendothelium,
modified
macrophages
leads
to
formation
foam
cells
storing
excess
amounts
cholesteryl
esters
subsequently
apoptosis.
This
review
describes
current
knowledge
about
metabolism
dyslipidemia
atherogenesis.
particular,
I
focus
effects
apolipoproteins,
lipid
composition
size
roles
cholesterol,
sphingomyelinase
apoB
denaturation
macrophage
cell
A
detailed
understanding
mechanisms
will
help
develop
new
therapeutic
strategies.
Nephrology Dialysis Transplantation,
Journal Year:
2014,
Volume and Issue:
29(8), P. 1554 - 1562
Published: Feb. 25, 2014
High-density
lipoprotein
(HDL)
confers
protection
against
atherosclerosis
by
several
different
mechanisms.
Although
in
the
general
population,
increasing
levels
of
HDL
are
associated
with
reduced
cardiovascular
(CV)
mortality,
this
association
is
not
well
known
patients
chronic
disease
states
such
as
end-stage
renal
disease.
We
hypothesize
that
serum
concentration
and
its
ratio
to
total
cholesterol
all-cause
CV
mortality
hemodialysis
from
population.
A
3-year
(July
2004
June
2007)
cohort
33
109
was
studied
USA
dialysis
clinics
where
lipid
profile
measured
at
least
50%
all
outpatients
clinic
during
a
given
calendar
quarter.
Cox
proportional
hazard
models
were
adjusted
for
demographics
case–mix
variables
cubic
splines
plotted.
Higher
concentrations
up
50
mg/dL
better
overall
survival,
while
60
above
rise
mortality.
All-cause
1.28
(1.20–1.38)
1.08
(1.01–1.16)
<30
1.05
(1.00–1.10)
(1.00–1.16)
≥
mg/dL,
respectively
(reference:
HDL:
30–<60
mg/dL).
In
contrast
low
higher
patients.
U-shaped
between
level
exists
<60
exhibiting
best
survival.
The
underlying
mechanisms
responsible
these
seemingly
paradoxical
associations
await
further
investigation.
International Journal of Vascular Medicine,
Journal Year:
2011,
Volume and Issue:
2012, P. 1 - 11
Published: Sept. 25, 2011
Postprandial
hyperlipidemia
with
accumulation
of
remnant
lipoproteins
is
a
common
metabolic
disturbance
associated
atherosclerosis
and
vascular
dysfunction,
particularly
during
chronic
disease
states
such
as
obesity,
the
syndrome
and,
diabetes.
Remnant
become
attached
to
wall,
where
they
can
penetrate
intact
endothelium
causing
foam
cell
formation.
activate
circulating
leukocytes,
upregulate
expression
endothelial
adhesion
molecules,
facilitate
migration
inflammatory
cells
into
subendothelial
space,
complement
system.
Since
humans
are
postprandial
most
day,
continuous
generation
remnants
after
each
meal
may
be
one
triggers
for
development
atherosclerosis.
Modulation
lipemia
by
lifestyle
changes
pharmacological
interventions
could
result
in
further
decrease
cardiovascular
mortality
morbidity.
This
paper
will
provide
an
update
on
current
concepts
concerning
relationship
between
lipemia,
inflammation,
function,
therapeutic
options.
International Journal of Molecular Sciences,
Journal Year:
2014,
Volume and Issue:
15(7), P. 12807 - 12841
Published: July 21, 2014
In
atherosclerosis;
blood
low-density
lipoproteins
(LDL)
are
subjected
to
multiple
enzymatic
and
non-enzymatic
modifications
that
increase
their
atherogenicity
induce
immunogenicity.
Modified
LDL
capable
of
inducing
vascular
inflammation
through
activation
innate
immunity;
thus,
contributing
the
progression
atherogenesis.
The
immunogenicity
modified
results
in
induction
self-antibodies
specific
a
certain
type
LDL.
antibodies
react
with
forming
circulating
immune
complexes.
Circulating
complexes
exhibit
prominent
immunomodulatory
properties
influence
atherosclerotic
inflammation.
Compared
freely
LDL;
associated
have
more
robust
atherogenic
proinflammatory
potential.
Various
lipid
components
may
serve
not
only
as
diagnostic
but
also
essential
predictive
markers
cardiovascular
events
atherosclerosis.
Accumulating
evidence
indicates
LDL-containing
can
biomarker
for
macrovascular
disease
1
diabetes.
Frontiers in Physiology,
Journal Year:
2020,
Volume and Issue:
11
Published: March 13, 2020
Wooden
breast
is
one
of
several
myopathies
fast-growing
commercial
broilers
that
has
emerged
as
a
consequence
intensive
selection
practices
in
the
poultry
breeding
industry.
Despite
substantial
economic
burden
presented
to
broiler
producers
worldwide
by
wooden
and
related
muscle
disorders
such
white
striping,
genetic
etiological
underpinnings
these
diseases
are
still
poorly
understood.
Here
we
propose
new
hypothesis
on
primary
causes
implicates
dysregulation
lipid
glucose
metabolism.
Our
addresses
recent
findings
have
suggested
etiologic
similarities
between
type
2
diabetes
despite
their
phenotypic
disparities.
Unlike
mammals,
metabolism
not
accompanied
an
increase
plasma
levels
but
generates
unique
skeletal
phenotype,
i.e.,
breast,
chickens.
We
hypothesize
disparities
result
from
major
difference
transport
birds
phenotype
most
closely
resembles
complications
smooth
cardiac
mammals.
Additional
basic
research
chickens
necessary
can
be
informative
for
production
well
human
health
disease.
To
inform
future
studies,
this
paper
reviews
current
biological
knowledge
outlines
steps
its
proposed
pathogenesis,
examines
how
traits
may
contributed
prevalence.