Apr 3, 1973 - Recent advances have been made in the elucidation of the mechanism of glycogen turnover in mammalian tissues. The present concept.
BIOLOGY
OF
272-278
9,
REPRODUCTION
Hormonal
(1973)
Regulation
of Rat Uterine
LAURENCE Department
M.
of Biochemistry,
DEMERS1 Upstate Syracuse,
AND
Glycogen
turnover in rat uterine the enzyme systems to immature (21-day-old)
level
treatment uterine in
glycogen
activity
in
consistent
with
face
of increased
h.
This
ovarian
rats
cause hypothesis
cell
activity
glycolysis
University
dependent
brought
changes that
JACOBS
D.
of New
York,
1973
(C-6-P)
steroidogenesis
the
uterine
3,
Metabolism
assessed under varying hormone conditions regulatory to glycogen metabolism. Estrogen rats brings about a significant increase in change is accompanied by statistical increases
glucose-6-phosphate
rat
female
immature
are
12
within
the
of
Elevations
ferase. to
deposition
levels
April
tissue was considered female
of
ROSS
Medical Center, State New York 13210
Accepted
at the
Glycogen
the
in
estrogen
form
about
by
glycogen
promotes
by augmenting
the
of
glycogen
cycle
uterine
levels
trans-
gonadotropin
treatment
which
enzymes,
glycogenesis
of the
in
glycogen
the
transferase
enzyme.
Recent elucidation turnover
advances have been made in the of the mechanism of glycogen in mammalian tissues. The
present
concept
breakdown leukocytes, of
two
(Leloir, and
anabolic volving transf
glycogen
distinct
1967; Wenger,
EC
pathway complex
phosphate Information
EC
of the 1965;
intact
rat
‘Present Hershey
rat and Bitman
to of
Address: Medical
Dept.
Center,
of
Hershey,
Pa.
© 1973 by of reproduction
The
Society in any
for form
the Study reserved.
organ.
S.
of
rat
uterus
by
Leonard
tivation
and
total uterus.
has
(1967)
estradiol
been
and
transferase
with
inactivation
not the
evi-
hormone phosphorylase
mammalian has of
the
investigated
is available mechanisms in
acin
biochemical
an elaborate uterine
concept in terms
markedly
Glycogenolysis extensively
turnover
have
treatment
will
glycogen
(1962)
enshown
Bo et al. rat
the
have
is increased in glycogen
that
the
the
enzyme increase
ovariectomized
tissue. This particularly
17033.
of Reproduction.
the
evidence
the
this
of
for
transferase
uterus
with
ad-
to these animals et al. (1965) have evidence
rat
activity
which
to
response
glycogen
enzyme system. Little information lates to the control
272 Copyright AU rights
the
glycogen M.
the
cycle. there is
estrus
rat,
glycogen,
in
Rubulis
dence to support cofactor-mediated
and In the
Pathology,
of
estradiol
of the
augment
concentrations
glycogen
uterus,
of
in
tivity
level
increased
of
provided
2.4.1.1.). available
mouse (Diamond et al., 1965).
low
normal spayed
biochemical
that the coincident
concerning hormonally induced biochemical changes associated with these rate-limiting glycogen metabolizing enzymes in the uterus Brody,
of
1952).
zyme
: ortho-
made
markedly
content
of glycogenolysis enzyme system
glucosyltransferase, has been
constant
is
presence
and
(-1,4-glucan
phosphorylase
a
provided
a-1,4-glucan 2.4.1.11)
the the
during
uterus
(Walaas,
path-
metabolism inenzyme glycogen
glucose:
cyclic
the
ministration
Lamer, 1966; Villar1967); (1) the
(UDP
catabolic by the
glycogen
heart, brain, assumes the
transferase,
erase
a-4-glucosyl
and
enzymatic
route of glycogen the rate-limiting
(2) the catalyzed
synthesis
in liver, muscle, and adipose tissue
existence ways Palasi
of
are
In
and
that realtering uterine
been defined, elaborate acprocesses
asso-
CLYCOCEN
UTERINE
with
ciated
the
of
the
during
ine
systems. This (1) investigate
individual
metabolizing
and
transferase
phorylase enzyme been designed to
forms
of
phos-
glycogenesis;
tionships
(2)
to study
between
the
and phosphorylase ing estrogen and to the immature
METHODS
time cycle
course enzymes
of inducfollow-
DiPietro comutase Both
Group
I.
the
(CFE
of
21-day-old
strain)
immature
were
fe-
administered
sub-
were
were
repeated
sacrificed
h following were
the
oil)
and
initial
h,
and
intervals
initial
treatment.
hormone
with
sacrificed
vehicle
at
zero
animals
Controls
injections
time
and
(sesame
96
h
within
group (1
mg/100
this
g)
estradiol (5 g/100 g) sc ing a 48-h priming period to determine if any correlated tween
these
over
in
Group male
two
l:he
ovarian
immature
II.
rats
A
group
(CFE
taneous
(100
to
the
increased
mals
were
were
content
of
induction in
72
of
the
response
to
steroidogenesis.
Ani-
time
appropriate
along
in
with
the
treated
intervals
animals.
30%
studies
KOH
The tissue
was
method glycogen digest
Tissue determined
described was with
using
by
Mont-
precipitated
alcohol
and
at
pH
activity
glucose-i-phosphate
systems
was
measured
regulated
to
a Cilford
determinations
that
or
were
either
added
hexokinase
cofactor.
and
as
gram
mea-
incubated
expressed per
Re-
were
without
for both
at
Bckman
phospho-
moles
tissue
pyridine
(wet
weight)
at 25#{176}C.
glucosyl Enzyme
the
transf
activity
erase
(synthe-
was
incorporation
quantitated
of
UDP-[”Clglucose
from
(1961)
Lamer
and
laboratories.
to
in
cofactor
the
‘#{176}C-labeled with
glycogen
by
the
homogenate
in 0.25
l
ture:
40
mrs
EDTA;
(when
of
and
mCi/mri) were reaction
taining
The isolated
in
a total
carried
out
terminated
1 mg LiBr above mixture by
the
was addition
prepared
primer; 2.4
mix-
7.5);
32
C-6-P
0.03
(specific volume for
of 0.3
15
1 mg
at
1 ml
30%
of
and ml
The precipitated glycogen was washed distilled water and the final precipitate
Incuba-
37#{176}C, and KOH
glycogen 2
Ci
activity ml.
mm
boiled
1,7
mrs
UDPC:
mrt
with
and
a low-speed
(pH
diphospho[U-”Clglucose
uridine
the initi-
reaction
buffer
glycogen
required);
of
following
tris-maleate 0.48%
of was
supernatant
the
to
l
in was
absence reaction
100
(5%)
sucrose mi
The
tissue
activity
and
G-6-P.
addition
uterine
to uterine
transferase
presence
metabolite
ated
modified
Clycogen
determined
147
glyco-
Mg’
subsequent isolation of the radioactive polysaccharide as “C-labeled glycogen. This isotope technique was first described by Villar-Palasi and
the
determination.
all
mm
dehydro-
hexokinase performed
and
attached
reduced
a
and MgCl2 as cofactors NADPH generated by
All
were
nucleotide
tions
of the
(1957).
a
and for
the ovarian and uterine organ at sacrifice. Control animals reinjection (normal saline) only
content
a modification
from
activity
our
Methods
Glycogen
gomery
fesubcu-
lU/animal)
enzymes at
ilnmature
combination
ovarian
sacrificed
Biochemical gen
(8
course
sacrificed
turn-
administered
in
cycle
as indicated with weights recorded ceived the vehicle and
Enzyme
groups be-
glycogen
21-day-old
FSH
endogenous
followtreatment
occurred
on
were
time
period
ATP, with
blanks
in generation
enzyme
reaction
substrate
(1948).
The was
in a thermostatically
against
a modifi-
(C-6-P)
NADP resulting
UDPG-glycogen tase) activity. by measuring
with
estrogen effect
of of
glycogen
48-h
a
of
lU/animal)
study
uterine
for
pro-
combination
uterus.
strain)
injections
HCC
in
steroids rat
received
series
sc
enzyme mu
using Najjar
NADPH
mixture. substrate
measured
glucomutase
post
to
NADP,
with The
without
per
A second
were
substrate pH 7.4.
sured
to 96
up
of
of
phosphoglu-
determined
phosphoglucomutase
Du Spectrophotometer corder Model 2000.
injection.
gesterone
h
24
every
at appropriate
maintained
presence
340
by
linked
system
method
The
were
the reaction glucose as
The
both
cutaneous injections of estradiol-17p (5 g/100 g) in sesame oil to study the time course of induction of enzymes rate limiting to glycogen turnover. Injections
at
(1960). determined
su-
activity kinetic
linear the
of
glucose-6-phosphate
in with
7.4.
Hexokinase
described
the
on
a 5% uterine
of under
systems
assay
levels
A group
rats
enzyme
phosphogluco-
performed
made
method
excess
as male
of the
with
Experiments
and
modification
and Weinhouse enzyme was
cation
in
a
solutions.
phosphoglucomutase
were
were
by
coupled
MATERIALS
a phenol-sulfuric
standard
assays
measurements conditions
erase
genase assay
AND
with
known
g supernatant fraction homogenate preparation.
crose
interrelatransf
and
enzyme
21,000
enzyme systems followgonadotrophin treatment female rat; and (3) to
establish the relative tion of the glycogen ing hormone treatment.
Animal
mutase
tissue uter-
the
uterine
colorimetrically
mixture
Uterine hexokinase and enzyme activities. Hexokinase
glycogen-
enzymes in rat uterine a period of hormone-induced
273
quantitated
acid
study has the status
the
METABOLISM
as the
concarrier.
glycogen
95%
ethanol. once
with
subjected
DEMERS
274 to
radioactive
of
“C
label
blanks
were
counting
to
incorporated processed
specimens
and
KOH
reagent
stop
estimate
into along
were
with
obtained
prior
the
glycogen. by
Ci
Control
mCi/mM
the
addition
30%
counting
Lient
temperature
liquid
scintillation
correction liquid
present
in an
(Model
with
cocktail
syst:m. of
napthalene,
0.4%
with
(1
(specific
ml
total
1 ml
mg/ml).
was
isolated
ner
similar
and
of
1
per
gram
Glycogen reverse
of
was
and [“Clglucose
labeled
The
featured into
glycogenolysis
[‘#{176}Clglucose-l-phosphate.
Glycogen mature
glucose
detennined
Enzyme
assay
of
based
on
activity absence
The
of
IN
low-speed
THE
following
the
the
uterine
ture
rat
No.
of
glycogen
of
estradiol-17/
has
a marked
in
to influ-
proliferation. biochemical
the
first
12 h fol-
treatment is the uterine As shown in Table 1, administration
begins
of
content
to rise
FEMALE
RATS
estradiol,
of the
above
imma-
control
levels
FOLLOWING
content
phosphorylase
(moles
glu/g/h)
+G-6-P
-G-6-P
(D)
g)
Glycogen
transferase
(Mrnoles
(mg/100
into
conmole
TREATMENT*
Glycogen
animals
rats
glycogen
1 IMMATURE
Glycogen
Hours
1
in tho Uterus of Imfollowing Estrogen
stimulated estrogen content.
OF
UTERUS
ESTROGEN
postinjection
kinetic to
uterine growth and the many anabolic
lowing glycogen
TABLE METABOLISM
transferase
equal
incorporated
female
parameters
the
reac-
supematant from a 5% uterine sucrose homogenate, 26 mrs C-i-P, 0.42% glycogen, 9.0 mM 5’-Amp (when required), 50 mrvr trismaleate buffer (pH 6.1), 0.01 as NaF, and 0.05
GLYCOGEN
the
controlled
administration
ence on Among
was of
The il
for
was
Metabolism Female Rats
21-day-old
x C)
(350
in a man-
counting
Administration
the incorporaglycogen from
determined in the presence and cof actor 5’-adenosine monophosphate. tion mixture as used contained 100
glyco-
RESULTS
tissue per hour.
activity.
phosphorylase
of
radioactive
of wet
phosphorylase
glycogen
tion
mole
reaction
2.5-
oxazole, and 0.020% dimethyl-2-2p-phenylene bis ( 5-phenyloxazole) all in a dioxane base of 15 ml total volume. Under the conditions of the assay, an enzyme unit corresponds to the into glycogen
the carrier
tissue per hour.
diphenyl
incorporation
were
polysaccharide
for
unit
glucose wet
and with
radioactive
established
radioactive
per gram
min
described
enzyme
200
Incubations
KOH
processed
that
Under an
10
30%
The
to
activity,
volume.
37#{176}C for
at
terminated
of
hy-
0.3
performed
ditions,
The
1.3%
in
enzyme.
150)
quench
consisted
0.6
am-
LS
automatic
for a [“C]dioxane
hyammne,
of
performed
Beckman
counter
scintillation
droxide
was
glucose-i-phosphate
gen
of tissue
supernate.
Radioactive
JACOBS
amount
all unknown adding
to the
AND
glu/g/h)
+AMP
(I)
-AMP
(t)
(a)
0 Control
9
131
+
12
6.3
+
.28
5.4
+
.20
1161
+
23
464
+
11
2
9
127
+
17
6.9
+
.33
5.0
+
.22
1061
+
18
386
+
17*
6
9
134
+
14
8.3
+
.32*
4.4
+
.21
966
+
14*
346
+
10*
12
260 325
+ +
22* 3Q*
10.3
+
.36*
5.0
+
.23
902
+
20*
321
+
14*
24
9 5
18.7
+
.87*
5.2
+
.18
1027
+
30
358
+
18*
48
5
318
+
27*
30.1
+
.50*
8.6
+
.27*
1250
+
47
593
+20*
72
5
270
+
24*
27.1
+
.62*
7.6
+
,34*
1412
+
43*
711
+
18*
96
5
252
+ 22*
29.0
+
.83*
+
1511
+
48*
817
+
25*
141
+
17
6.6
+
.24
9.0 5.7
+
.29
1204
+
32
486
+
22
24 Progesterone&
-
280
+
27*
27.8
+
.84*
7.2
+
.63*
1372
+
47*
844
+
34*
48 Progesteron&’
-
261
+
19*
26.0
+
.92*
8.0
+
55*
1463
+
40*
893
+
26*
96 Control
The
in
9
#{176}
II
the
absence
of
to
enzyme
in
the
(t)
refers
measured Results
form
G-6-P
Statistically
transferase
from
as mean
different
this
calculated
enzyme
measured
of
treatment
was
total
activity
absence
expressed
Progesterone *
of glycogen
in
by subtracting
activity the
measured
presence
of
in 5’-AMP,
35*
the activity the
presence while
the
of transferase of G-6-P. (a)
form
is that
cofactor.
±SE. given
in combination
at P < 0.01
level
with
as compared
estradiol
to control.
folowing
48-h
estrogen
measured
Phosphorylase
prime.
activity
UTERINE
between 6 and 12 treatment, reaching after initial hormone creased lowed
following maximum injection.
estrogen 24-48 h This in-
glycogen deposition was then by a progressive decline, which
continuous
through
the
content,
dependent
form
was
folwas
elevation
the (D)
of
observed
in
uterine
to
glycogen
be
creased be
form
of the
slightly
tween
the
through
at which time were over four
of the control form of glycogen other
hand,
during which induced
showed
animals
initial
vehicle
possibility
that
enzyme
of
control
did
not
uterine
same
changes
(total assessed
sponse
to
first
12
estrogen
with
whether tissues This
both
or
to
h
of
treatment,
was
treatment.
phosphorylase
At
slight
activity were values. activity
These were
steroidogenesis
glycogen
ture
female
treatment
on ovaries
with
was
increased
rat imma-
immature
The were
combination
and
trophin
of
metabolism. rat
a
through
attempt
effects
stimulated
gonadotrophin
human
chorionic
gonado-
follicle-stimulating
hormone
simultaneously.
Figure
1
900 000ry
0
rethe
400
in
fresh protein.
followed 24
HrS
by and
h post-estrogen both
an
study, the
system,
between of
particular observe
consis-
gram
then
increased
on
Immature
eoo
decline was
enzyme
48
Treatment in the
AMP)
-
course
in units per per milligram levels
control
own
During
of this
control the
the
active
decrease
to
enzyme
which
forms
phosphorylase
rats
estrogen-induced observed
pattern
of study.
time
a
this
conditions,
and
was
expressed in units
slight
a return
nor-
second
essentially
There of the
period
the
activity,
In made
administered
initial
process. weight
treatment.
there
phosphorylase tent
AMP
the
the
phosphosylase +
h
and
the
immature
the
during
h,
out
from
experimental
glycogen
were
from result
during
the
at
by
Uterus
ovarian
96
content
maturation in uterine
animals
rule
glycogen
of the
changes
Under
to
at
the
Metabolism
uterine
both
and
observed
levels
reproductive were no
evaluated
injection
development
from
in activity
injection
the
changes
control
48
change
were
time
following
mal
little
studies
in the was
of Gonadotrophin
Rat
reported
96 h of treatment.
Effects
the
the
as
administered
enzyme
Glycogen
independent (I), on
beforms.
with
estrogen
on
both ratio
enzyme
treatment
effect
glycogen-cycle
the first 24 h of hormone treatment, could be correlated to the estrogenuterine glycogenesis.
Control the
animals. The transferase
total
with
(-AMP)
increased
Progesterone of
active
between
consistent
(1962).
without
the enzyme times that
an
It
the
enzyme
and
was
period
treatment.
1 that
phosphorylase
simultaneously
estro-
h post
elevation in
finding
increase
gen treatment, activity levels
Table
active
uterine
48-h
to 48 h following
96
on greater
resulting
but significantly at 6 h following initiation of estrogen treatment. This glycogen transferase activity continued to show a steady in activity
and
phosphorylase
the
Leonard
transfer-
72
noted
forms,
on
elevated
at
may
This
glucose-6-phosphate
275
METABOLISM
showed
96 h.
Accompanying glycogen ase
h a
GLYCOCEN
forms
further
1.
of in in-
Effect
of
with
weights
significantly elevations
Fic. treatment
sults
are
trol
weights
the
mean
time
from expressed
as
taken
value
goiiadotrophin on
treated
as
of
oj.
post
(FSH-HCC) and
uterine
21-day-old
female
percent
of
100%.
Each
14
weights
were
26 ±
3 mg,
weights
were
81 ± 6 mg
animals. while each.
ovarian
control point
Control the
control
tissue rats. with
Recon-
represents
ovarian uterine
DEMERS
276
AND
JACOBS 24
36
Hrs.
not o,J.
48
72
GIycoeo
FIG.
2.
Time
cycle
enzymes
tions
from
course
initiation
change
from
was
calculated
glucose-8-phosphate Control values hexokinase, 918
3.7 21
in
weight
cogen cycle
reproductive
ovarian
weight
as well as the were evaluated
gonadotrophin ing the initial in
Fig.
treatment hormone
2, the
tive
uterine
glycogen
statistically
of
the
metabolic In
the
glycogen following
content
at
delayed
this
significantly h post-horof hexowere also time,
increases
observed
gonadotrophin dependent slightly post-treatment--a
as
early
treatment; form elevated
of
as
the
enzyme 48
time
period
30
h
account
for
curring
at
activities
as
activity
cofactor
phosphorylase,
mutase,
phosphogluco-
phosphorylase.
the 48
as
increased
h. both
glycogenesis
Glycogen
immature
return mone
to control treatment.
oc-
phosphorylase declined
forms
observed
treated
with
slightly
the
animals
estrogen-
with
levels by All enzyme
and gonadotrophin in terms of units
a
gradual
72 h post-horchanges in the of
study activity
as per gave
were per
gram fresh similar ac-
patterns.
The
homeostatic
in-
in
the
of intensive
tems brain,
h
to
mechanism
metabolism
subject years.
tigations
only late
24-96 h percent
from
plotted
glycogen
PC
of
initially
cent
72
are
total
glycogen
tivity
post-
was and
sacrificed
milligram protein as well tissue. Both measurements
of
the
glycogen
determina-
DISCUSSION
levels transferase
too
total
uterine
whereas
between
and
indica-
in
increased activity form of glycogen
were
hexokinase;
estrogen evaluated
after
activity.
contrast, dependent
were
utergly-
up to 96 h followinjection. As shown
a considerable lag phase was elevated between 36 and 48 mone treatment. The activities kinase and phosphoglucomutase
increased
as
Eleva-
uterine
in the presence of this cofactor. glycogen, 122 ± 11 (mg/100 g); 7.6 ± 0.32 (moles/g/m); total
measured
glu/g/h); used: hex,
weight
control.
in
of duplicate
Results
following:
Phosphor,
preceded the Changes in uterine
change.
content, enzymes,
transferase;
organ
Animals
phosphoglucomutase, (moles
changes
as 0%. The percent I transferase measured in the absence of the
taken
the
Phosphor.
the mean
intervals.
activity
Abbreviations
the
represents uteri.
activity
(moles/gna/m);
glycogen
from
three
.GT
induced
bar
selected
the transferase parameter were
glu/g/h).
change
of
at
7.7 ± 0.32
(moles
the
percent tions
0.22
UDPC-Ct,
mutase;
ine
±
a pool
treatment
the control animals percent of enzyme
over each
for
transferase,
±
shows
with
as that
Each
rats.
assay
UDPG
(FSH-HCC)
female of
control
PGoase
gonadotrophin
each
assays,
the
glycogen
of
21-day-old
in four
following
He
under and
mammalian
the
of glycogen
cofactors
from
rate-limiting turnover
and cardiac the homeostatic (Leloir,
glycogen has
investigation
It is apparent that
of tissues
and
these enzyme
in liver,
been
in reinvessysmuscle,
adipose tissue are control of hormones 1967;
Lamer,
1966).
GLYCOGEN
UTERINE
In
consideration
an
of the
attempt
was
influence,
to
lion
elucidate
the
in glycogen metabolism of the imrat uterus by measuring the activity glycogen turnover enzymes, glycogen
changes
mature of the
transferase,
and
under
glycogen
differing
relative
of
systems
sion
two
periods
genesis
has
Williams gested with transferase
of
increased
been
studied.
and
Provine
cogerlesis.
event
No
evidence
further
has
glyco-
have a dependent independent to the
in
kinetic transferase
Sug-
data
gly-
support
literature.
of (D
the indiand I) on
purified muscle and liver preparations, independent form is considered to active
form
responsible
transfer glycogen.
of
relative glycogen
distribution transferase
tissue
for
glucose units It has also been of is
concentration
forth, 1965; a reciprocal
the two a function
et
be
forms of
glycogen
ine
glycogenesis
rat,
as
in
well
treated
as
no
transferase
count
for
uterine
the
in
the
enzyme, observed
with
which early
glycogenesis.
consistent
animals,
This
the
report
Provine (1966), who tions in the independent
the
lack
to of the
hormonal transferase
meta-
take
place
under
certain
where the transf erase not become elevated,
activity
of
the
related (Adrouny,
O’Toole,
1969;
Recently
dependent
form glyco-
1969; Wiley
Goldberg
and
published
laboratory
I acand
to increased
synthesis
Leveille,
observations
on human
cycle
is
the
by
endometrium
of
following
ment,
suggesting
cogen
itself
and
steady
state
of
the
in
pendent
gly-
zyme
uterine these
temporal
pattern
period.
enzyme,
activa-
dependent (AlT)
Further derway
activation
systems the
5’-AMP
decline 48 the
enzyme
studies assess
ininde-
in this whether
en-
after
h,
in terms
between
exert The
phosphorylase
after
48
h
is sugfor the observed
since
there
of the
activity
transferase
systems
a be-
which
turnover.
occurring
agreement
gly-
of
condition
content
studies
to
by
treatment (Table 1) the responsible factor
glycogen
eletreat-
establishment
enzyme
and
relationship
and
equilibrium
between
seen
enzyme acthe early
hormonal
the
ratio
and
1969). may be
glycogenesis
glycogen
fornIS
phosphorylase
With
two
changes
(Demers
possible
post-estrogen gested to be in
closely
prolonged
over
activity
stimulation.
increased
vated
creased
and
parallels deposition
uterine phosphorylase are depressed during
tivities phases
acin-
which
glycogen
in
control
small elevawhich pre-
transferase glycogenesis
in
can
closely
1970).
events tissue glyco-
and
tween
of Williams
glvcogenic
muscle, brain, and adipose the concept that enhanced
gen
form
increases
detected form
between the dependent level and the uterine response
on estrogen. studies on
the
that
ceded uterine glycogenesis in the adult ovariectomized animal. On the other hand, we have demonstrated a close correlation
in
transferase enzyme is rate limituterine glycogen synthesis and is
is more
there could
finding
glythe
Jacobs, 1969; Hughes et a!., In Table 1 and Fig. 2, it
female
independent
syn-
of the
gonadotrophin-
female
changes
of the
on
dependent
strual
uter-
immature
studies
immature
were
the
with
to the
is, the
I form and the glycogen content. In our studies on estrogen-induced
the
for
and
cogen transferase activity show that the dependent transferase activity has a cyclic activity pattern during the normal men-
(Dan-
a!., 1969). That exists between
in
conditions level does
our
accounting
observed
the the
catalytic
from UDPG shown that
of
Huijing relationship
the
bolic tivity
I shift)
paralleling the uterine rise, it is suggested that
content
dependent ing to
to
increases enzyme
where
for uterine
appeared
the known forms of
large
genesis (1966)
responsible
concept
the
cardiac support
forms
uterine
(D
glycogenesis
dependent Recent
interconver-
their findings that conversion to an
is the
The
enzyme
early
cogen
principal
of an
individual
during
From vidual
these
in terms
between
form
conditions.
277
process
the thetase
phosphorylase
hormonal
activity
enzyme
this
hormonal
made
METABOLISM
at
is and
this
laboratory are the uterine
time unde-
DEMEBS
278
pendent crease de
transferase is a function
novo
protein
gested
for
enzyme activity of estrogen-induced
synthesis,
several
key
as
in-
JACOBS glucan
tion
recently
glycolytic
AND
and
sug-
of
enzymes.
insulin
LARNER,
C.
ADROUNY, glycogen
A.
(1969).
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metabolism
in
cardiac
patterns and
of
skeletal
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(1969).
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after
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Hepatic
L.,
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WEINHOUSE,
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on
the
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transferase
con-
S.,
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control
N.
COLDBERG,
F.,
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of glycogen
synthesis-
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F.
(1967).
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