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A random Abstract
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11β-HSD1 is the major regulator of the tissue-specific effects of circulating glucocorticoid excess.
[cushing syndrome]
The
adverse
metabolic
effects
of
prescribed
and
endogenous
glucocorticoid
(
GC
)
excess
,
Cushing
syndrome
,
create
a
significant
health
burden
.
We
found
that
tissue
regeneration
of
GCs
by
11
β-hydroxysteroid
dehydrogenase
type
1
(
11
β-
HSD
1
)
,
rather
than
circulating
delivery
,
is
critical
to
developing
the
phenotype
of
GC
excess
;
11
β-
HSD
1
KO
mice
with
circulating
GC
excess
are
protected
from
the
glucose
intolerance
,
hyperinsulinemia
,
hepatic
steatosis
,
adiposity
,
hypertension
,
myopathy
,
and
dermal
atrophy
of
Cushing
syndrome
.
Whereas
liver
-
specific
11
β-
HSD
1
KO
mice
developed
a
full
Cushingoid
phenotype
,
adipose-
specific
11
β-
HSD
1
KO
mice
were
protected
from
hepatic
steatosis
and
circulating
fatty
acid
excess
.
These
data
challenge
our
current
view
of
GC
action
,
demonstrating
11
β-
HSD
1
,
particularly
in
adipose
tissue
,
is
key
to
the
development
of
the
adverse
metabolic
profile
associated
with
circulating
GC
excess
,
offering
11
β-
HSD
1
inhibition
as
a
previously
unidentified
approach
to
treat
Cushing
syndrome
.
Diseases
Validation
Diseases presenting
"hepatic steatosis"
symptom
adrenal incidentaloma
aromatase deficiency
cushing syndrome
werner syndrome
x-linked adrenoleukodystrophy
zellweger syndrome
This symptom has already been validated