J Appl Physiol 95: 1132-1138, 2003.
First published May 9, 2003; doi:10.1152/japplphysiol.01172.2002
8750-7587/03 $5.00
Prior exercise enhances passive absorption of intraduodenal glucose
R. Richard Pencek,
Yoshiharu Koyama,
D. Brooks Lacy,
Freyja D. James,
Patrick T. Fueger,
Kareem Jabbour,
Phillip E. Williams, and
David H. Wasserman
Department of Molecular Physiology and Biophysics, Diabetes Research and
Training Center, and Department of Surgery, Vanderbilt University School of
Medicine, Nashville, Tennessee 37232-0615
Submitted 20 December 2002
; accepted in final form 5 May 2003
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ABSTRACT
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The purpose of this study was to assess whether a prior bout of exercise
enhances passive gut glucose absorption. Mongrel dogs had sampling catheters,
infusion catheters, and a portal vein flow probe implanted 17 days before an
experiment. Protocols consisted of either 150 min of exercise (n = 8)
or rest (n = 7) followed by basal (-30 to 0 min) and a primed (150
mg/kg) intraduodenal glucose infusion [8.0 mg ·
kg-1 · min-1, time
(t) = 0-90 min] periods. 3-O-[3H]methylglucose
(absorbed actively, facilitatively, and passively) and
L-[14C]glucose (absorbed passively) were injected into
the duodenum at t = 20 and 80 min. Phloridzin, an inhibitor of the
active sodium glucose cotransporter-1 (SGLT-1), was infused (0.1 mg ·
kg-1 · min-1) into the
duodenum from t = 60-90 min with a peripheral venous isoglycemic
clamp. Duodenal, arterial, and portal vein samples were taken every 10 min
during the glucose infusion, as well as every minute after each tracer bolus
injection. Net gut glucose output in exercised dogs increased compared with
that in the sedentary group (5.34 ± 0.47 and 4.02 ± 0.53 mg
· kg-1 · min-1).
Passive gut glucose absorption increased 
100% after exercise (0.93
± 0.06 and 0.45 ± 0.07 mg · kg-1
· min-1). Transport-mediated glucose absorption
increased by 20%, but the change was not significant. The infusion of
phloridzin eliminated the appearance of both glucose tracers in sedentary and
exercised dogs, suggesting that passive transport required SGLT-1-mediated
glucose uptake. This study shows 1) that prior exercise enhances
passive absorption of intraduodenal glucose into the portal vein and
2) that basal and the added passive gut glucose absorption after
exercise is dependent on initial transport of glucose via SGLT-1.
dogs; phloridzin; splanchnic blood flow
EXERCISE ENHANCES THE ABILITY of insulin to stimulate skeletal
muscle (25) and liver
(22) glucose uptake. This
increase in insulin sensitivity, however, does not uniformly lead to improved
oral glucose tolerance (15,
18,
24). Work done by Hamilton et
al. (9) showed that failure to
improve oral glucose tolerance, despite increased insulin-stimulated glucose
uptake, is due to increased absorption of glucose from the gut. The resulting
enhancement in splanchnic bed glucose output counterbalances the effect of
increasing muscle glucose uptake on arterial glucose levels.
The mechanism by which prior exercise enhances the absorption from the gut
is unknown. Gut glucose absorption is both transporter mediated and passive.
Transporter-mediated gut glucose absorption occurs via luminal sodium glucose
cotransporter-1 (SGLT-1) Na+-K+ active transporters
(5,
10) and GLUT-2-mediated
facilitated diffusion. Facilitated diffusion of glucose occurs when transport
of glucose via SGLT-1 stimulates translocation of GLUT-2 transporters to the
luminal surface of the gut
(11,
16). Transporter-mediated
glucose transport encompasses 90% of total gut glucose absorption in both
conscious dogs (17,
23) and rats
(31,
32). The remaining 10% of gut
glucose absorption is due to paracellular diffusion across the intestinal
wall, although this route also appears to be indirectly dependent on
intestinal SGLT-1-mediated glucose transport, at least in sedentary, conscious
dogs (23).
The purpose of the present study is to determine whether the increased
absorption of intraduodenal glucose after exercise is due to increased
transporter-mediated and/or passive glucose absorption. For this purpose,
3-O-[3H]methylglucose (absorbed via active, facilitative,
and passive routes) and L-[14C]glucose (absorbed
passively) were delivered in trace amounts in the duodenum to determine the
contributions of transporter-mediated and passive pathways to net gut glucose
absorption during an intraduodenal glucose load
(3,
4).
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MATERIALS AND METHODS
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Animal care and surgical procedures. Fifteen mongrel dogs of
either sex, with a mean weight of 23 ± 1 kg, were studied. A subset of
the sedentary dogs was published previously
(23). The dogs were housed in
a facility that met the American Association for the Accreditation of
Laboratory Animals Care guidelines. All procedures were approved by the
Vanderbilt University Animal Care and Use Committee. The dogs were fed a
standard diet of meat and chow (34% protein, 14.5% fat, 46% carbohydrate, and
5.5% fiber based on dry weight).
At least 16 days before each experiment, a laparotomy was performed under
general anesthesia. Two Silastic catheters (0.03 mm ID) were inserted into the
inferior vena cava for indocyanine green (ICG) and glucose infusions. Silastic
catheters (0.04 mm ID) were inserted into the portal vein and left common
hepatic vein for blood sampling, as described previously
(36). Two Silastic catheters
(0.03 mm ID) were inserted into the duodenum. The first catheter was inserted
just below the pyloric sphincter for administration of glucose, phloridzin,
3-O-[3H]methylglucose, and
L-[14C]glucose. The second duodenal catheter was
inserted just before the junction of the duodenum with the jejunum (10 cm
caudal to the first duodenal catheter). A Silastic catheter (0.03 mm ID) was
inserted into the left femoral artery for blood sampling. After insertion, the
vascular catheters were filled with saline containing heparin and knotted at
the free ends.
Transonic flow probes (Transonic Systems, Ithaca, NY) were used to measure
portal vein blood flow (PVF), as described previously
(23). The flow probe lead and
knotted catheter ends were stored in a subcutaneous pocket made in the
abdominal region. The femoral artery catheter was stored in a pocket in the
inguinal region. One week before an experiment, dogs for either protocol were
trained to run on a treadmill (4 mph on a 12% grade). Training consisted of
20-, 40-, and 90-min bouts to acclimate the dogs to treadmill exercise. Dogs
were not exercised 48 h before an experiment. Only those animals that met the
following criteria were used in this study: a leukocyte count
<18,000/mm3, a hematocrit >0.36, normal stools, and a good
appetite (consuming the entire daily ration). Animals meeting these criteria
were fasted 18 h before the beginning of the study to ensure that all animals
were postabsorptive.
Experimental protocol. The experimental protocol is shown in
Fig. 1. On the day of the
experiment, the catheters and flow probes were freed from subcutaneous pockets
by using 2-cm incisions made after application of 2% lidocaine. Saline
was infused into the arterial sampling catheter throughout the duration of the
study. Dogs were submitted to 150 min of moderate treadmill exercise
(n = 8; 4 mph, 12% grade) or an equivalent period of rest in a Pavlov
stand [n = 7; time (t) = -190 to -40 min]. At t =
-110 min, a venous infusion of ICG was initiated and was continued for the
duration of the study. This infusion served as a backup measurement of
splanchnic blood flow in case the transonic flow probes did not function
properly. It was assumed, based on previous work
(9), that PVF is 80% of
splanchnic blood flow, whereas hepatic artery blood flow represents the other
20%. ICG was used as a substitute for transonic flow probes in 3 of the 15
experiments. At t = -40 min, exercised dogs were transferred to a
Pavlov harness for the remainder of the study. From t = -30 to 0 min,
blood samples were taken for baseline measurements. Because the duodenum was
empty during this period, no duodenal sample could be obtained. The
experimental period (t = 0-90 min) began with the injection of a 150
mg/kg body wt glucose primer (20% dextrose) into the duodenum, followed by a
continuous intraduodenal glucose infusion of 8 mg ·
kg-1 · min-1 (20% dextrose)
until t = 90 min. The rate of the intraduodenal glucose infusion was
chosen to reproduce glucose levels commonly seen in the portal vein after
feeding. At t = 20 min, a bolus containing trace amounts of
3-O-[3H]methylglucose and
L-[14C]glucose (25 µCi of each isotope) was injected
into the duodenum. At t = 60 min, an intraduodenal bolus of
phloridzin (1.97 mg/kg) was given, followed by a continuous intraduodenal
phloridzin infusion of 0.1 mg · kg-1 ·
min-1 for the remainder of the study. At the start of
the phloridzin infusion, an isoglycemic clamp was initiated to maintain the
arterial glucose concentration at the level seen before phloridzin infusion.
At t = 80 min, a second bolus of
3-O-[3H]methylglucose and
L-[14C]glucose (100 µCi of each isotope), fourfold
larger than the first, was introduced into the duodenum. During the
experimental period, blood and duodenal samples were taken every 10 min. In
addition to these samples, blood and duodenal samples were taken every minute
for 5 min after administration of each tracer bolus. Because
D-glucose and 3-O-methylglucose are transported out of the
lumen, less of these sugars makes it to the paracellular gaps, compared with
L-glucose. Consequently, gradients in the ratios of
3-O-[3H]methylglucose to
L-[14C]glucose exist. Although these gradients are
impossible to measure directly, evidence suggests that they are minimal during
the period immediately after the bolus, as direct and indirect measures of
luminal sugar ratios give the same result
(23). It has been shown in our
previous work (23) that
determination of the passive fraction of gut glucose absorption using this
technique is quantitatively the same as is seen in the work of Lane et al.
(17), which measured the
absorption of L-glucose isotopes in isolated perfused jejunal
sections over a 2-h period. At the end of the experiment, animals were
euthanized with pentobarbital sodium, and an autopsy was performed to confirm
catheter and flow probe placement.
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Fig. 1. Experimental protocol. Arrows indicate the injection of a tracer bolus [25
µCi at time (t) = 20 min and 100 µCi at t = 80 min] of
3-O-[3H]methylglucose and
L-[14C]glucose into the duodenum. Arterial plasma
glucose levels were clamped from t = 60-90 min to match
concentrations from t = 20-60 min.
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Blood and intraduodenal sample analyses. Plasma and intraduodenal
glucose levels were determined on the day of the experiment by using the
glucose oxidase method with a Beckman Glucose Analyzer II (Beckman
Instruments, Fullerton, CA). ICG absorption was assessed in arterial and
hepatic vein plasma samples at 810 nm after centrifugation (3,000 g,
30 min). Those plasma samples that were not immediately analyzed were stored
at -70°C for later analysis. Whole blood and intraduodenal samples were
deproteinized with barium hydroxide and zinc sulfate to assess the
radioactivity of 3-O-[3H]methylglucose and
L-[14C]glucose in blood and duodenal samples. After
centrifugation (3,000 g,30 min), the supernatant was dried and
reconstituted in 1 ml of water and 10 ml Ultima Gold scintillent (Packard,
Meriden, CT). Radioactivity was determined by using a Packard TRI-CARB 2900TR
liquid scintillation counter. Plasma insulin and glucagon and blood glucose
were measured as described previously
(9).
Calculations. Total net gut glucose output (NGGO) was calculated
as described by Eq. 1
 | (1) |
where [P] and [A] are portal vein and arterial glucose concentrations,
respectively. NGGO during the duodenal glucose infusion is represented as the
average NGGO from t = 20-60 min. Calculations of the
transporter-mediated and passive components of gut glucose absorption are
based on tracer data obtained during the 5 min of sampling after
administration of the tracer bolus. Previous work has shown that the
calculation of the passive fraction of gut absorption via both direct and
indirect assessment of intraduodenal radioactivity yields the same results
(23). The direct approach was
used in the present study (Eq. 2) to calculate the passive fraction
of gut glucose absorption
Fraction of gut glucose absorption that is passive
 | (2) |
where L-GlcP and L-GlcA are the
portal venous and arterial radioactivity of
L-[14C]glucose, respectively; MGP and
MGA are the radioactivities of
3-O-[3H]methylglucose in the portal vein and the artery,
respectively; and MGD and L-GlcD are the
duodenal concentrations of 3-O-[3H]methylglucose and
L-[14C]glucose, respectively. The rates of
transporter-mediated and passive absorption were calculated by multiplying the
fraction of passive and transporter-mediated absorption by NGGO (Eqs.
3 and 4, respectively).
Net rate of transporter-mediated absorption
 | (3) |
Net rate of passive absorption
 | (4) |
Statistics. All data presented herein are means ± SE. ANOVA
was performed to assess differences between gut absorption, hormone, and
substrate concentrations in sedentary and exercised dogs. Differences were
considered significant if P < 0.05.
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RESULTS
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Arterial blood glucose, glucose infusion rates, plasma hormones, and
PVF. Arterial blood glucose concentrations were not significantly
different in exercised (75 ± 3 mg/dl) and sedentary (82 ± 2
mg/dl) dogs during the basal period (Fig.
2). Arterial blood glucose levels rose to similar levels in both
exercised (110 ± 7 mg/dl) and sedentary (113 ± 5 mg/dl) dogs
during the intraduodenal glucose infusion. After the administration of
phloridzin, arterial blood glucose levels were maintained at levels seen
before phloridzin administration with the peripheral glucose clamp (107
± 6 exercised vs. 107 ± 5 mg/dl sedentary). The glucose infusion
rate required to maintain isoglycemia was not different in exercised and
sedentary dogs (5.19 ± 0.70 vs. 4.67 ± 0.48 mg ·
kg-1 · min-1).
Arterial plasma insulin was significantly less in exercised compared with
sedentary dogs (4 ± 1 vs. 7 ± 1 µU/ml) during the baseline
period, whereas glucagon was significantly higher (50 ± 5 vs. 33
± 6 ng/ml). During intraduodenal glucose infusion in the absence of
phloridzin, insulin rose approximately threefold in each group but remained
significantly lower in exercised compared with sedentary (15 ± 3 vs. 24
± 5 µU/ml) dogs. Arterial plasma glucagon in exercised and sedentary
dogs was not different during intraduodenal glucose infusion (40 ± 6
vs. 30 ± 5 ng/ml). Plasma cortisol levels were significantly higher in
the baseline period in exercised dogs (5.4 ± 0.9 vs. 2.4 ± 1.7
pg/ml). During the intraduodenal glucose infusion, plasma cortisol levels were
similar between groups (3.8 ± 0.9 vs. 3.9 ± 0.7 pg/ml).
Catecholamines were not different between groups in the baseline period or
during the intraduodenal glucose infusion. Hormone levels, in the presence of
phloridzin, were not different between groups.
PVF during the baseline period was significantly higher in exercised dogs
(25 ± 3 vs. 18 ± 2 ml · kg-1
· min-1). However, PVF was not different during
the intraduodenal glucose infusion period in the presence (24 ± 2 vs.
23 ± 4ml · kg-1 ·
min-1) or absence (27 ± 2 vs. 21 ± 3 ml
· kg-1 · min-1,
exercised vs. sedentary dogs) of phloridzin.
NGGO, net transporter-mediated and net passive glucose output.
NGGO was negative in both rested and exercised dogs during the baseline
period, reflecting net gut uptake of glucose from the blood
(Fig. 3). During the first 60
min of the intraduodenal glucose load, NGGO rose in the sedentary group,
averaging 4.02 ± 0.53 mg · kg-1 ·
min-1. Prior exercise caused a significant increase in
NGGO in the presence of intraduodenal glucose (5.36 ± 0.46 mg ·
kg-1 · min-1). This
increase in NGGO was, in part, due to a 65% increase in the percent
contribution of passive gut glucose absorption to total NGGO, which was
11% in sedentary dogs and 18% in exercised dogs
(Fig. 4). This increase in the
percent contribution of passive absorption was reflected by a doubling in the
net rate of passive gut glucose absorption (0.93 ± 0.06 vs. 0.45
± 0.07 mg · kg-1 ·
min-1). The rate of transporter-mediated absorption
increased 20% with exercise but was not significantly different from that
in sedentary dogs (4.41 ± 0.45 vs. 3.57 ± 0.48 mg ·
kg-1 · min-1). After the
administration of phloridzin, NGGO decreased in both sedentary and exercised
dogs, so that rates in neither group were significantly different from zero
(Fig. 3).
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Fig. 3. Net gut glucose output (NGGO) in sedentary (open bars) and exercised (solid
bars) dogs during the baseline sampling period and intraduodenal glucose
infusion period in the presence (+) and absence (-) of phloridzin. Negative
values represent the uptake of glucose from the blood by the gut, whereas
positive values represent absorption of glucose from the gut. Values are means
± SE. *P < 0.05 vs. sedentary.
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Fig. 4. A: percent contribution of passive absorption to NGGO in sedentary
(open bars) and exercised (solid bars) dogs as calculated by using Eq. 2.
B: rate of passive gut glucose absorption calculated by using Eq.
4. Values are means ± SE. *P < 0.05 vs.
sedentary.
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DISCUSSION
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It was shown previously that absorption of intraduodenal glucose is
accelerated after a bout of prolonged, moderate-intensity exercise
(9). The increased gut glucose
absorption facilitates the delivery of glucose to glycogen-depleted tissues
(liver and muscle), accelerating replenishment of these stores. The method
presented here is an extension of the method described by Uhing and Kimura
(32) that we have previously
adapted for use in the dog model
(23). The experimental
protocol takes advantage of arteriovenous and duodenal sampling techniques, as
well as isotopic tracer methodology to determine the contributions of
transporter-mediated and passive processes to the absorption of an
intraduodenal glucose load in sedentary and exercised dogs. The components of
gut glucose absorption have also been measured by the disappearance of glucose
analogs from the gut (6,
17). Measuring passive
absorption via this technique is difficult, because it is a relatively small
component of total gut absorption and is reliant on the disappearance of a
small fraction of the passive absorption marker from the gut. The appearance
of tracers in the portal vein was used to calculate the contributions of
passive and transporter-mediated processes to total gut glucose absorption.
This method was first described by Uhing and Kimura
(31) and adapted for use in
the dog (23). The advantage of
this for determination of passive transport is that, at the time of the first
bolus, absorption of the passive marker, L-[14C]glucose,
occurs on a background of zero and is relatively easy to detect. The
appearance of tracers in the portal vein was assessed over a short interval
after delivery of the bolus. This was done to minimize gradients in the ratio
of tracers in the duodenal lumen. It should be noted that this technique gives
the same results for the percent contribution of passive gut glucose
absorption as previous work done by Lane et al.
(17), in which isolated
jejunal segments were perfused for 2 h.
The present studies and previous work
(17,
23,
32) assessing passive gut
glucose absorption have used L-glucose as a marker for the passive
process. A considerable volume of work suggests that L-glucose does
not interact with the SGLT-1 transporter
(6,
13,
17,
32). For example, in
basolateral membrane vesicles isolated from rat small intestine, the presence
of 100 mM L-glucose did not inhibit radioactive
D-glucose uptake, suggesting that L-glucose does not
interact with the transporter
(38). Work done by Ikeda et
al. (13), using vesicles
isolated from rabbit small intestine and Xenopus oocytes expressing a
cloned version of SGLT-1, showed with competition experiments that
L-glucose had no effect on D-glucose uptake. However,
results of a study in the rat led to the conclusion that L-glucose
is not a valid marker for passive gut glucose absorption
(26). It was suggested in this
study that differences existed in the gut absorption of L-glucose
compared with other nonmetabolized hexoses. It should be noted that gut
absorption of the hexoses was determined by their subsequent urine collection.
This is an indirect assessment of intestinal absorption and can be affected by
differential renal handling
(33). Additionally, if
L-glucose had a significant, but minor, affinity for the SGLT-1
transporter and the changes in gut glucose absorption with exercise could be
ascribed completely to transporter-mediated absorption, then the increase in
what we describe as the passive component should be accompanied by a large and
unambiguous increase in transport-mediated gut glucose absorption.
Nevertheless, one cannot rule out from the present study that there is a
fraction of L-glucose that is transported, and this possibility
must be considered.
The work presented here shows that the increase in NGGO after exercise is
accompanied by an increase in passive gut glucose absorption. Whereas the
increase in transporter-mediated gut glucose absorption was not significant,
it did tend to be higher as well. Despite this tendency for an increase in
transporter-mediated absorption, its actual percent contribution to NGGO was
decreased. We observed only a 24% nonsignificant increase in
transporter-mediated absorption. A power analysis indicated that we had the
power to detect a 50% change in transporter-mediated gut glucose absorption
with a power of 0.95, with n = 7, assuming equal variance between
groups. It should be noted, however, that, based on our subject number and the
observed variance between groups, there is a 18% chance that a type II
statistical error occurred, which could have resulted in failure to detect a
significant difference between groups. In both sedentary and exercised dogs,
NGGO was less than the infusion rate of glucose into the duodenum. The
differences between the infusion rate and NGGO can be attributed to glucose
metabolism by the gut and delayed absorption of glucose over time
(1). Previous work in the dog
has shown that, when a glucose load is delivered to the gut, 15-18% of
that load is metabolized by the gut itself
(1,
19). Additionally, previous
work in the conscious dog model showed that, in the presence of an
intraduodenal glucose infusion, there was a gradual increase in
tracer-determined gut glucose absorption over time that approached the
duodenal infusion rate
(19).
There are several possible mechanisms for this increase in passive NGGO
during an intraduodenal glucose load. Metabolic stresses such as exercise
(9) and fasting
(7) result in increased NGGO
during an intraduodenal glucose load. These conditions are characterized by an
increase in gut proteolysis, which serves to increase gluconeogenic substrate
supply to the liver (8). This
increased proteolysis could impair the gut's ability to function as a barrier
during feeding when it follows such a physiological stress.
Exercise is characterized by changes in circulating hormone levels, which
result in increased production of glucose to meet the increasing energy
demands of the body. There are several potential endocrine responses that are
known to occur during exercise that, as a result of prolonged exposure during
exercise, could potentially affect nutrient absorption in response to
subsequent feeding. It has been reported that 
-adrenergic stimulation of
the small intestine in rats
(14) and sheep
(2) by epinephrine results in
increased gut glucose absorption. The primary target of such stimulation has
been postulated to be the SGLT-1 transporter. It is conceivable that this
increase in catecholamines seen during prolonged exercise could enhance gut
glucose absorption during feeding after exercise. Whereas a significant
increase in transporter-mediated absorption was not observed, in the present
study we do show that the passive component of gut glucose absorption under
both sedentary and exercised conditions is indirectly dependent on SGLT-1
stimulation. In addition to the potential role of epinephrine in stimulating
gut glucose absorption, the elevation in plasma glucocorticoid concentrations
during exercise (27) could
also conceivably lead to an enhancement in NGGO during an intraduodenal
glucose load. Dexamethasone treatment in conscious rats increased the
absorption of glucose by the gut after the delivery of an oral glucose load
(29). Additionally, work done
in rabbits has shown that the injection of dexamethasone can increase gut
glucose absorption for extended periods of time after this treatment
(12). During prolonged
exercise, glucagon levels rise, whereas insulin decreases
(35). Previous work has shown
that elevated insulin levels increase gut glucose absorption
(30), whereas increased levels
of glucagon cause a delay in absorption
(28). The intraduodenal
glucose infusion still resulted in increased NGGO in exercised dogs, despite
the prolonged exposure to reduced insulin, which persisted into the glucose
infusion period, and elevated glucagon levels. In addition to the potential
impact of these exercise-induced hormonal changes, the impact of exercise on
splanchnic blood flow could potentially lead to alterations in gut absorption
in the postexercise state. Previous work has shown that the changes in blood
flow alter gut glucose absorption
(34,
37). After the period of
exercise or rest, PVF was significantly higher in exercised compared with
sedentary dogs. During the intraduodenal glucose infusion, PVF was comparable
in both groups. Even though blood flow was similar in both groups, potential
changes in the microcirculation of the blood vessels perfusing the gut could
facilitate the absorption of glucose from the gut.
In sedentary dogs, the delivery of a tracer bolus in the presence of
phloridzin does not result in an increase in circulating radioactivity of
either isotope, indicating an impairment of passive as well as
transporter-mediated absorption. This finding is consistent with previous work
that showed that a requisite amount of active transport is required for
passive transport to occur
(20,
21). In exercised dogs, where
passive glucose absorption is enhanced, absorption of both glucose analogs is
still inhibited by phloridzin administration, indicating that the enhanced
passive glucose absorption after exercise is also dependent on
transport-mediated gut absorption. This suggests that the same fundamental
processes are involved.
Transporter-mediated and passive gut glucose absorption have been
calculated by using both direct and indirect estimates of intraduodenal
glucose analog radioactivity because of inherent difficulties in duodenal
sampling (23). In previous
work that describes these calculations, there was no significant difference
between the results obtained using different calculation methods
(23). In this experiment, only
data from the calculation of the passive fraction by using direct duodenal
sampling are presented. It should be noted that the passive fraction was
calculated by using equations both reliant on and independent of direct
duodenal sampling and that there was no difference between results obtained
with different calculation methods (data not shown).
After exercise, the delivery of an intraduodenal glucose load resulted in
an increase in total NGGO. This was accompanied by a 65% increase in the
percent contribution of the passive component of gut glucose absorption and an
associated 100% increase in the mass of glucose absorbed by the passive
process. Intraduodenal infusion of phloridzin, an inhibitor of the SGLT-1
transporter, completely abolishes NGGO during an intraduodenal glucose load in
sedentary dogs. Here we show that NGGO during an equivalent glucose load is
also not significantly different from zero in the presence of phloridzin in
exercised dogs. Additionally, the absorption of
L-[14C]glucose after the administration of the second
tracer bolus was completely eliminated. These findings indicate that the added
passive gut glucose absorption in the postexercise state is also dependent on
a requisite rate of transporter-mediated gut glucose absorption.
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DISCLOSURES
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This work was funded by National Institute of Diabetes and Digestive and
Kidney Diseases Grant RO1 DK-50277, Diabetes Center Grant DK-20593, and
Training Grant 5-T32-DK-7563-08.
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ACKNOWLEDGMENTS
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We thank Deanna Bracy for valued assistance with the completion of this
work, as well as the Vanderbilt University Diabetes Center Hormone Assay Core
for contribution to this work.
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FOOTNOTES
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Address for reprint requests and other correspondence: R. R. Pencek, Dept. of
Molecular Physiology and Biophysics, Vanderbilt Univ. School of Medicine,
Nashville, TN 37232-0615 (E-mail:
r.r.pencek{at}vanderbilt.edu).
The costs of publication of this article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section 1734
solely to indicate this fact.
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Copyright © 2003 by the American Physiological Society.
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ABSTRACT
MATERIALS AND METHODS
) and exercised
(
) dogs during the baseline sampling period (-30 to 0 min) and during
the intraduodenal glucose infusion in the absence (0-60 min) or presence
(60-90 min) of intraduodenal phloridzin. Values are means ± SE.