The
epidemic
of
obesity,
type
2
diabetes
and
nonalcoholic
liver
disease
(NAFLD)
favors
drug
consumption,
which
augments
the
risk
adverse
events
including
injury.
For
more
than
30
years,
a
series
experimental
clinical
investigations
reported
or
suggested
that
common
pain
reliever
acetaminophen
(APAP)
could
be
hepatotoxic
in
obesity
related
metabolic
diseases,
at
least
after
an
overdose.
Nonetheless,
several
did
not
reproduce
these
data.
This
discrepancy
might
come
from
extent
steatosis,
accumulation
specific
lipid
species,
mitochondrial
dysfunction
diabetes-related
parameters
such
as
ketonemia
hyperglycemia.
Among
factors,
some
them
seem
pivotal
for
induction
cytochrome
P450
2E1
(CYP2E1),
conversion
APAP
to
toxic
metabolite
N-acetyl-p-benzoquinone
imine
(NAPQI).
In
contrast,
other
factors
explain
why
NAFLD
are
always
associated
with
frequent
severe
APAP-induced
acute
hepatotoxicity,
increased
volume
distribution
body,
higher
hepatic
glucuronidation
reduced
CYP3A4
activity.
Accordingly,
occurrence
outcome
injury
obese
individual
would
depend
on
delicate
balance
between
augment
generation
NAPQI
others
can
mitigate
hepatotoxicity.
Frontiers in Endocrinology,
Год журнала:
2024,
Номер
14
Опубликована: Янв. 8, 2024
Nonalcoholic
fatty
liver
disease
(NAFLD)
affects
approximately
30%
of
individuals
globally.
Both
serum
glucose
and
albumin
were
demonstrated
to
be
potential
markers
for
the
development
NAFLD.
We
hypothesized
that
risk
NAFLD
may
proportional
glucose-to-albumin
ratio
(GAR).
Nutrition Reviews,
Год журнала:
2024,
Номер
unknown
Опубликована: Янв. 12, 2024
Clinical
evidence
from
investigations
of
the
effects
curcumin
on
liver
enzymes
in
patients
with
nonalcoholic
fatty
disease
(NAFLD)
have
led
to
inconsistent
results.
The
epidemic
of
obesity,
type
2
diabetes
and
nonalcoholic
liver
disease
(NAFLD)
favors
drug
consumption,
which
augments
the
risk
adverse
events
including
injury.
For
more
than
30
years,
a
series
experimental
clinical
investigations
reported
or
suggested
that
common
pain
reliever
acetaminophen
(APAP)
could
be
hepatotoxic
in
obesity
related
metabolic
diseases,
at
least
after
an
overdose.
Nonetheless,
several
did
not
reproduce
these
data.
This
discrepancy
might
come
from
extent
steatosis,
accumulation
specific
lipid
species,
mitochondrial
dysfunction
diabetes-related
parameters
such
as
ketonemia
hyperglycemia.
Among
factors,
some
them
seem
pivotal
for
induction
cytochrome
P450
2E1
(CYP2E1),
conversion
APAP
to
toxic
metabolite
N-acetyl-p-benzoquinone
imine
(NAPQI).
In
contrast,
other
factors
explain
why
NAFLD
are
always
associated
with
frequent
severe
APAP-induced
acute
hepatotoxicity,
increased
volume
distribution
body,
higher
hepatic
glucuronidation
reduced
CYP3A4
activity.
Accordingly,
occurrence
outcome
injury
obese
individual
would
depend
on
delicate
balance
between
augment
generation
NAPQI
others
can
mitigate
hepatotoxicity.
