Diabetes,
Journal Year:
2018,
Volume and Issue:
67(5), P. 818 - 830
Published: Feb. 23, 2018
Type
2
diabetes
mellitus
(T2DM)
has
become
one
of
the
most
serious
and
long-term
threats
to
human
health.
However,
molecular
mechanism
that
links
obesity
insulin
resistance
remains
largely
unknown.
Here,
we
show
F-box
WD
repeat
domain-containing
7
(FBXW7),
an
E3
ubiquitin
protein
ligase,
is
markedly
downregulated
in
liver
two
obese
mouse
models
subjects.
We
further
identify
a
functional
low-frequency
FBXW7
coding
variant
(p.Ala204Thr)
Chinese
population,
which
associated
with
elevated
blood
glucose
T2DM
risk.
Notably,
mice
liver-specific
knockout
develop
hyperglycemia,
intolerance,
even
on
normal
chow
diet.
Conversely,
overexpression
not
only
prevents
development
high-fat
diet–induced
but
also
attenuates
disease
signature
mice.
Mechanistically,
directly
binds
hepatokine
fetuin-A
induce
its
ubiquitination
subsequent
proteasomal
degradation,
comprising
important
maintaining
homeostasis.
Thus,
provide
evidence
showing
beneficial
role
Nutrients,
Journal Year:
2020,
Volume and Issue:
12(6), P. 1899 - 1899
Published: June 26, 2020
Exercise
is
an
effective
strategy
for
preventing
and
treating
obesity
its
related
cardiometabolic
disorders,
resulting
in
significant
loss
of
body
fat
mass,
white
adipose
tissue
browning,
redistribution
energy
substrates,
optimization
global
expenditure,
enhancement
hypothalamic
circuits
that
control
appetite-satiety
decreased
systemic
inflammation
insulin
resistance.
Novel
exercise-inducible
soluble
factors,
including
myokines,
hepatokines,
osteokines,
immune
cytokines
adipokines
are
hypothesized
to
play
important
role
the
body’s
response
exercise.
To
our
knowledge,
no
review
has
provided
a
comprehensive
integrative
overview
these
novel
molecular
players
mechanisms
involved
metabolic
fuel
during
after
exercise,
weight
reduced
inflammation.
In
this
review,
we
explain
potential
namely
such
as
irisin,
IL-6,
IL-15,
METRNL,
BAIBA,
myostatin,
particular
selenoprotein
P,
fetuin
A,
FGF21,
ANGPTL4,
follistatin.
We
also
describe
function
specifically
osteocalcin,
leptin,
adiponectin,
resistin.
emphasize
pleiotropic
mechanisms,
pathways,
inter-organ
crosstalk
mass
loss,
inflammation,
healthy
induced
by
Journal of Clinical Investigation,
Journal Year:
2019,
Volume and Issue:
129(10), P. 4032 - 4040
Published: Sept. 8, 2019
Obesity
originates
from
an
imbalance
between
caloric
intake
and
energy
expenditure
that
promotes
adipose
tissue
expansion,
which
is
necessary
to
buffer
nutrient
excess.
Patients
with
higher
visceral
fat
mass
are
at
a
risk
of
developing
severe
complications
such
as
type
2
diabetes
cardiovascular
liver
diseases.
However,
increased
does
not
fully
explain
obesity's
propensity
promote
metabolic
With
chronic
obesity,
undergoes
major
remodeling,
can
ultimately
result
in
unresolved
inflammation
leading
fibrosis
accumulation.
These
features
drive
local
damage
initiate
and/or
maintain
multiorgan
dysfunction.
Here,
we
review
the
current
understanding
remodeling
focus
on
obesity-induced
its
relevance
clinical
manifestations.
International Journal of Molecular Sciences,
Journal Year:
2018,
Volume and Issue:
19(12), P. 3720 - 3720
Published: Nov. 22, 2018
The
incidence
of
metabolic
disorders,
including
diabetes,
has
elevated
exponentially
during
the
last
decades
and
enhanced
risk
a
variety
complications,
such
as
diabetes
cardiovascular
diseases.
In
present
review,
we
have
highlighted
new
insights
on
complex
relationships
between
diet-induced
modulation
gut
microbiota
diabetes.
Literature
from
various
library
databases
electronic
searches
(ScienceDirect,
PubMed,
Google
Scholar)
were
randomly
collected.
There
exists
relationship
diet
microbiota,
which
alters
energy
balance,
health
impacts,
autoimmunity,
further
causes
inflammation
dysfunction,
Faecalibacterium
prausnitzii
is
butyrate-producing
bacterium,
plays
vital
role
in
Transplantation
F.
been
used
an
intervention
strategy
to
treat
dysbiosis
gut’s
microbial
community
that
linked
inflammation,
precedes
autoimmune
disease
review
focuses
literature
highlights
benefits
especially,
abundant
protecting
pattern
its
therapeutic
potential
against
Annual Review of Physiology,
Journal Year:
2021,
Volume and Issue:
84(1), P. 135 - 155
Published: Nov. 9, 2021
Obesity
is
a
chronic
and
progressive
process
affecting
whole-body
energy
balance
associated
with
comorbidity
development.
In
addition
to
increased
fat
mass,
obesity
induces
white
adipose
tissue
(WAT)
inflammation
fibrosis,
leading
local
systemic
metabolic
dysfunctions,
such
as
insulin
resistance
(IR).
Accordingly,
limiting
or
fibrosis
deposition
may
improve
IR
glucose
homeostasis.
Although
no
targeted
therapy
yet
exists
slow
reverse
number
of
findings
have
clarified
the
underlying
cellular
molecular
mechanisms.
this
review,
we
highlight
remodeling
events
shown
be
deposition,
focus
on
progenitors
involved
in
obesity-induced
healthy
well
unhealthy
WAT
expansion.
Frontiers in Cell and Developmental Biology,
Journal Year:
2022,
Volume and Issue:
10
Published: July 18, 2022
Fetuin-A
is
a
heterodimeric
plasma
glycoprotein
containing
an
A-chain
of
282
amino
acids
and
B-chain
27
acid
residues
linked
by
single
inter-disulfide
bond.
It
predominantly
expressed
in
embryonic
cells
adult
hepatocytes,
to
lesser
extent
adipocytes
monocytes.
binds
with
plethora
receptors
exhibits
multifaceted
physiological
pathological
functions.
involved
the
regulation
calcium
metabolism,
osteogenesis,
insulin
signaling
pathway.
also
acts
as
ectopic
calcification
inhibitor,
protease
inflammatory
mediator,
anti-inflammatory
partner,
atherogenic
factor,
adipogenic
among
other
several
moonlighting
has
been
demonstrated
play
crucial
role
pathogenesis
disorders.
This
review
mainly
focuses
on
structure,
synthesis,
biological
roles
fetuin-A.
Information
was
gathered
manually
from
various
journals
Immunity Inflammation and Disease,
Journal Year:
2020,
Volume and Issue:
9(1), P. 59 - 73
Published: Dec. 17, 2020
Abstract
Low‐level
of
chronic
inflammation
activation
is
characteristic
obesity.
Nonalcoholic
fatty
liver
disease
(NAFLD)
closely
linked
to
obesity
and
an
emerging
health
problem,
it
originates
from
abnormal
accumulation
triglycerides
in
the
liver,
sometimes
causes
inflammatory
reactions
that
could
contribute
cirrhosis
cancer,
thus
its
pathogenesis
needs
be
clarified
for
more
treatment
options.
Once
NAFLD
established,
contributes
systemic
inflammation,
low‐grade
continuously
maintained
during
causing
impaired
resolution
obesity,
which
subsequently
exacerbates
severity.
This
study
focuses
on
effects
obesity‐induced
inflammations,
are
underlying
progression
development
severe
fibrotic
stages.
Understanding
relationship
between
help
establishing
attractive
therapeutic
targets
or
diagnostic
markers
response
provides
new
approaches
prevention