Nature Metabolism,
Journal Year:
2022,
Volume and Issue:
4(2), P. 190 - 202
Published: Feb. 14, 2022
Abstract
The
mechanisms
promoting
disturbed
white
adipocyte
function
in
obesity
remain
largely
unclear.
Herein,
we
integrate
adipose
tissue
(WAT)
metabolomic
and
transcriptomic
data
from
clinical
cohorts
find
that
the
WAT
phosphocreatine/creatine
ratio
is
increased
creatine
kinase-B
expression
activity
decreased
obese
state.
In
human
vitro
murine
vivo
models,
demonstrate
phosphocreatine
metabolism
adipocytes
alters
adenosine
monophosphate-activated
protein
kinase
via
effects
on
triphosphate/adenosine
diphosphate
levels,
independently
of
beigeing.
This
disturbance
promotes
a
pro-inflammatory
profile
characterized,
part,
by
chemokine
(C-C
motif)
ligand
2
(CCL2)
production.
These
suggest
system
links
cellular
energy
shuttling
with
responses
adipocytes.
Our
findings
provide
unexpected
perspectives
driving
inflammation
may
present
avenues
to
target
dysfunction.
Cell Metabolism,
Journal Year:
2021,
Volume and Issue:
33(9), P. 1869 - 1882.e6
Published: Aug. 10, 2021
The
contribution
of
cellular
heterogeneity
and
architecture
to
white
adipose
tissue
(WAT)
function
is
poorly
understood.
Herein,
we
combined
spatially
resolved
transcriptional
profiling
with
single-cell
RNA
sequencing
image
analyses
map
human
WAT
composition
structure.
This
identified
18
cell
classes
unique
propensities
form
organized
homo-
heterotypic
clusters.
Of
these,
three
constituted
mature
adipocytes
that
were
similar
in
size,
but
distinct
their
spatial
arrangements
profiles.
Based
on
marker
genes,
termed
these
AdipoLEP,
AdipoPLIN,
AdipoSAA.
We
confirmed,
independent
datasets,
respective
gene
profiles
associated
differently
both
adipocyte
whole-body
insulin
sensitivity.
Corroborating
our
observations,
stimulation
vivo
by
hyperinsulinemic-euglycemic
clamp
showed
only
AdipoPLIN
displayed
a
response
insulin.
Altogether,
mining
this
multimodal
resource
identify
composed
adipocytes,
one
which
responsive.
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: March 8, 2021
Tissue-resident
macrophages
(TRMs)
are
heterogeneous
populations
originating
either
from
monocytes
or
embryonic
progenitors,
and
distribute
in
lymphoid
non-lymphoid
tissues.
TRMs
play
diverse
roles
many
physiological
processes,
including
metabolic
function,
clearance
of
cellular
debris,
tissue
remodeling
defense.
Macrophages
can
be
polarized
to
different
functional
phenotypes
depending
on
their
origin
microenvironment.
Specific
macrophage
subpopulations
associated
with
disease
progression.
In
studies
fate-mapping
single-cell
RNA
sequencing
methodologies,
several
critical
molecules
have
been
identified
induce
the
change
function.
These
potential
markers
for
diagnosis
selective
targets
novel
macrophage-mediated
treatment.
this
review,
we
discuss
some
recent
findings
regarding
less-known
new
functions
well-known
molecules.
Understanding
mechanisms
these
has
yield
treatments
diagnostic
approaches
disease.
Angiogenesis,
Journal Year:
2022,
Volume and Issue:
25(4), P. 439 - 453
Published: July 20, 2022
Abstract
While
most
tissues
exhibit
their
greatest
growth
during
development,
adipose
tissue
is
capable
of
additional
massive
expansion
in
adults.
Adipose
expandability
advantageous
when
temporarily
storing
fuel
for
use
fasting,
but
becomes
pathological
upon
continuous
food
intake,
leading
to
obesity
and
its
many
comorbidities.
The
dense
vasculature
provides
necessary
oxygen
nutrients,
supports
delivery
from
adipocytes
under
fed
or
fasting
conditions.
Moreover,
the
comprises
a
major
niche
multipotent
progenitor
cells,
which
give
rise
new
are
repair.
Given
multiple,
pivotal
roles
vasculature,
impairments
angiogenic
capacity
may
underlie
obesity-associated
diseases
such
as
diabetes
cardiometabolic
disease.
Exciting
studies
on
single-cell
single-nuclei
composition
mouse
humans
providing
insights
into
mechanisms
angiogenesis.
modes
intercellular
communication
involving
micro
vesicle
exosome
transfer
proteins,
nucleic
acids
organelles
also
being
recognized
play
key
roles.
This
review
focuses
cellular
signaling
underlying
angiogenesis,
impact
pathophysiological
consequences.
