Adipose tissue-derived microRNA-450a-5p induces type 2 diabetes mellitus by downregulating DUSP10
Molecular Biomedicine,
Год журнала:
2025,
Номер
6(1)
Опубликована: Фев. 6, 2025
Abstract
Type
2
diabetes
mellitus
(T2DM)
has
rapidly
increased
worldwide,
emerging
as
the
fifth
leading
cause
of
death.
The
treatment
T2DM
is
challenging
due
to
side
effects
oral
hypoglycemic
drugs
and
limited
efficacy
long-term
insulin
therapy,
which
can
lead
resistance
(IR).
Consequently,
there
significant
in
discovering
new
that
have
minimal
a
pronounced
effect.
In
obesity,
microRNA
levels
been
implicated
glucose
metabolism
disorders
T2DM,
although
many
aspects
remain
unresolved.
Here,
we
confirmed
visceral
adipose
tissue
serum
microRNA-450a-5p
content
under
obesity
it
was
significantly
positively
associated
with
fasting
blood
glucose,
triglycerides,
cholesterol,
low-density
lipoproteins-cholesterol
subjects.
high-fat
diet
(HFD)-induced
obese
mice,
expression
serum,
liver,
white
tissue.
Moreover,
Dicer
-knockout
mouse
model
constructed
identify
main
source
microRNA-450a-5p.
could
inactivate
signal
pathway
by
targeting
inhibited
Dual
Specificity
Phosphatase
10
(DUSP10)
inducing
IR
vitro
cultured
hepatocytes
adipocytes.
Additionally,
found
regulate
DUSP10
signaling
activity,
influencing
tolerance
sensitivity
across
various
models,
including
normal
diet,
HFD-induced
obese,
tissue-specific
microRNA-450a-5p-knockout,
db/db
mice.
Furthermore,
gallic
acid
might
play
potential
role
inhibiting
decreasing
expression.
Thus,
emerges
an
attractive
therapeutic
target
for
addressing
IR,
T2DM.
Язык: Английский
Role of manganese in brain health and disease: focus on oxidative stress
Free Radical Biology and Medicine,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 1, 2025
Язык: Английский
Combining vinpocetine or cocoa with levodopa, Coenzyme Q10 and vitamin B complex mitigates rotenone-induced Parkinson’s disease in rats: Impact on Nrf2/HO-1, NF-kB, AMPK/SIRT-1/Beclin-1, AKT/GSK-3β/CREB/BDNF and Apoptotic Pathways
Biomedicine & Pharmacotherapy,
Год журнала:
2025,
Номер
186, С. 118011 - 118011
Опубликована: Март 31, 2025
Язык: Английский