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Amino acid absorption and homeostasis in mice lacking the intestinal peptide transporter PEPT1.
[cystinuria]
The
intestinal
peptide
transporter
PEPT
1
mediates
the
uptake
of
di
-
and
tripeptides
derived
from
dietary
protein
breakdown
into
epithelial
cells
.
Whereas
the
transporter
appears
to
be
essential
to
compensate
for
the
reduced
amino
acid
delivery
in
patients
with
mutations
in
amino
acid
transporter
genes
,
such
as
in
cystinuria
or
Hartnup
disease
,
its
physiological
role
in
overall
amino
acid
absorption
is
still
not
known
.
To
assess
the
quantitative
importance
of
PEPT
1
in
overall
amino
acid
absorption
and
metabolism
,
PEPT
1
-
deficient
mice
were
studied
by
using
brush
border
membrane
vesicles
,
everted
gut
sacs
,
and
Ussing
chambers
,
as
well
as
by
transcriptome
and
proteome
analysis
of
intestinal
tissue
samples
.
Neither
gene
expression
nor
proteome
profiling
nor
functional
analysis
revealed
evidence
for
any
compensatory
changes
in
the
levels
and
/
or
function
of
transporters
for
free
amino
acids
in
the
intestine
.
However
,
most
plasma
amino
acid
levels
were
increased
in
Pept
1
(
-
/
-
)
compared
with
Pept
1
(
+
/
+
)
animals
,
suggesting
that
amino
acid
handling
is
altered
.
Plasma
appearance
rates
of
(
15
)
N-
labeled
amino
acids
determined
after
intragastric
administration
of
a
low
dose
of
protein
remained
unchanged
,
whereas
administration
of
a
large
protein
load
via
gavage
revealed
marked
differences
in
plasma
appearance
of
selected
amino
acids
.
PEPT
1
seems
,
therefore
,
important
for
overall
amino
acid
absorption
only
after
high
dietary
protein
intake
when
amino
acid
transport
processes
are
saturated
and
PEPT
1
can
provide
additional
absorption
capacity
.
Since
renal
amino
acid
excretion
remained
unchanged
,
elevated
basal
concentrations
of
plasma
amino
acids
in
PEPT
1
-
deficient
animals
seem
to
arise
mainly
from
alterations
in
hepatic
amino
acid
metabolism
.
Diseases
Validation
Diseases presenting
"deficient animals"
symptom
cystinuria
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