Acarbose, an ␣-Glucosidase Inhibitor, Attenuates

Postprandial Hypotension in Autonomic Failure

Cyndya Shibao, Alfredo Gamboa, Andre Diedrich, Cynthia Dossett, Leena Choi,
Ginnie Farley, Italo Biaggioni

Abstract—Postprandial hypotension is an important clinical condition that predisposes to syncope, falls, angina, and
cerebrovascular events. The magnitude of the fall in blood pressure after meals depends on enteric glucose availability.
We hypothesized that acarbose, an ␣-glucosidase inhibitor that decreases glucose absorption in the small intestine,
would attenuate postprandial hypotension. Acarbose or placebo was given 20 minutes before a standardized meal in 13
patients with postprandial hypotension in the setting of autonomic failure (age: 65⫾2.64 years; body mass index:
25⫾1.08 kg/m2; supine plasma norepinephrine: 110⫾26.6 pg/mL). Four patients were studied in a single-blind protocol
and 9 patients in a double-blind, randomized, crossover fashion. Patients were studied supine, and blood pressure, heart
rate, and neuroendocrine parameters were obtained at baseline and for 90 minutes after meal intake. After adjusting for
potential confounders, acarbose significantly attenuated the postprandial fall in systolic and diastolic blood pressures
by 17 mm Hg (95% CI: 7 to 28; P⫽0.003) and 9 mm Hg (95% CI: 5 to 14; P⫽0.001), respectively. Furthermore,
acarbose effectively reduced plasma levels of insulin, a known vasodilator, by 11 ␮U/mL (95% CI: 5 to 18;
P⫽0.001) compared with placebo. After adjusting for insulin levels, the attenuation of postprandial hypotension
by acarbose remained significant, indicating that additional mechanisms contribute to this effect. In conclusion,
100 mg of acarbose successfully improved postprandial hypotension in patients with severe autonomic failure. This
effect is not explained solely by a reduction in insulin levels. (Hypertension. 2007;50:54-61.)
Key Words: postprandial 䡲 hypotension 䡲 acarbose 䡲 ␣-glucosidase inhibitor
䡲 autonomic nervous system diseases 䡲 autonomic failure

P ostprandial hypotension (PPH), defined as a fall in

systolic blood pressure (SBP) of ⬎20 mm Hg occurring
within 2 hours after a meal,1,2 is an important clinical problem
that predisposes to syncope, falls, angina pectoris, and cere-
brovascular events.3,4 The clinical presentation is character-
ized by symptoms of lightheadedness with an onset within 30
minutes after food ingestion.5 The magnitude of the decrease
in blood pressure depends on the size of the meal6 and its
composition4,7; PPH is more severe the greater the carbohy-
drate content.8 Those most affected are patients with some
degree of autonomic impairment, suggesting that, in healthy
subjects, the hypotensive effect of meals is buffered by the
autonomic nervous system. PPH has been reported in healthy
elderly persons,9,10 elderly patients with hypertension,11–13
elderly residents of nursing homes,14,15 patients with Parkin-
son disease,16 –18 and patients with diabetes mellitus.19 PPH is
particularly severe in patients suffering from primary forms
of autonomic failure.1
The pathogenesis of PPH is likely multifactorial. Gastro-
intestinal and pancreatic hormones with vasodilatory proper-
ties seem to play a key role. These are released into the
bloodstream in response to food intake and are responsible
for pooling of blood in the splanchnic circulation.20 Notably,
drugs that blunt the release of these hormones, for example,
octreotide,21 or that antagonize their action, for example,
caffeine,22 attenuate PPH and are integral components of the
treatment strategy for this condition.
Recently, it has been proposed that acarbose, commonly
used to control postprandial hyperglycemia in type 2 diabetes
mellitus,23 could potentially improve PPH. Acarbose inhibits
␣-glucosidase in the brush border of the small intestine,
delaying glucose absorption by decreasing the breakdown of
complex carbohydrates. These actions have been shown to
decrease the release of gastrointestinal hormones including
insulin, a known vasodilator.
Two case reports found improvement of PPH in patients
with type 124 and type 225 diabetes mellitus. Furthermore,
Maruta et al26 showed that voglibose, another ␣-glucosidase
inhibitor, also attenuates PPH in patients with neurologic

Received March 25, 2007; first decision April 13, 2007; revision accepted April 29, 2007.
From the Department of Medicine, Division of Clinical Pharmacology and the Autonomic Dysfunction Center (C.S., A.G., A.D., G.F., I.B.), General
Clinical Research Center (C.D.), and the Department of Biostatistics (L.C.), Vanderbilt University School of Medicine, Nashville, Tenn.
This work was part of ClinicalTrials.gov: http://www.clinicaltrials.gov/ct/show/NCT00223691;jsessionid⫽968AF1FB9496078B5C1308983B16CB
BD?order⫽2, NCT00223691.
Correspondence to Italo Biaggioni, 1500 21st Ave South, Suite 3500, Clinical Trials Center, Vanderbilt University, Nashville, TN 37212. E-mail
Italo.biaggioni@vanderbilt.edu
© 2007 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org DOI: 10.1161/HYPERTENSIONAHA.107.091355

54
 Shibao et al
disorders, such as multiple system atrophy and Parkinson
disease. Although these findings are promising, further stud-
ies are needed to support the use of acarbose for the treatment
of PPH because of the lack of randomization and placebo
control in previous reports. Thus, the aim of our study was to
evaluate the effectiveness of acarbose for the treatment of
PPH in patients with severe autonomic failure.
Methods
Study Population
A total of 13 patients with severe autonomic failure secondary to
postganglionic neuronal denervation (12 with pure autonomic failure
and 1 with Parkinson disease) were recruited from referrals to the
Autonomic Dysfunction Center at Vanderbilt University. PPH was
defined as a fall of ⱖ20 mm Hg in SBP within 2 hours after meal
intake.27 Patients were excluded if they had secondary causes of
autonomic failure (eg, diabetes mellitus or amyloidosis) or if
acarbose was contraindicated (eg, abnormal liver function or Crohn
disease). The criteria of the American Autonomic Society was used
to ascertain the diagnosis of pure autonomic failure.28 The study was
approved by the institution review board at Vanderbilt University,
and all of the subjects gave informed consent.
Experimental Protocol
All of the subjects were admitted to Vanderbilt University General
Clinical Research Center. Subjects were fed a low monoamine,
caffeine-free diet containing 150 mEq of sodium and 60 to 80 mEq
of potassium per day for ⱖ3 days before evaluation. Medications
affecting the autonomic nervous system were withheld for ⱖ5
half-lives before admission. Patients were studied in 3 different days,
a screening day and 2 study days (day 1 and day 2), for the
medication trials.
Screening
All of the participants underwent an initial screening phase. Auto-
nomic function tests were performed to evaluate the integrity of
autonomic reflex arcs. These included the Valsalva maneuver, cold
pressor test, isometric handgrip, and sinus arrhythmia (change in
heart rate [HR] in response to controlled breathing).29 All of the tests
were standardized previously in our laboratory.30
To diagnose PPH, a hypotensive breakfast test with a standardized
meal (414 calories, 14 g of protein, 51.7 g of carbohydrates, and
16.8 g fat) was performed. Brachial blood pressure and HR were
measured using an automated sphygmomanometer (Dinamap, GE
Medical Systems Information Technologies) for 30 minutes at
baseline while seated and for 120 minutes after meal intake.31
An orthostatic test was performed to evaluate hemodynamic and
hormonal changes on standing. An indwelling catheter was placed in
an antecubital vein to obtain blood samples while patients remained
supine after an overnight rest. Subjects were asked to stand as long
as possible or for ⱖ10 minutes. During this period, they were
allowed to sit at intervals if presyncopal symptoms developed.
Brachial blood pressure and HR were measured, and blood samples
for catecholamine determinations were obtained while supine
and standing.
Medication Trial
The study was conducted in the morning after an overnight fast and
in the postvoid state. To assess the tolerability of acarbose in our
patients, the effect of 100 mg of acarbose (Bayer Pharmaceuticals
Corporation) was first studied on a single-blind, nonrandomized,
crossover design (day 1, placebo; day 2, 100 mg of acarbose) in 4
patients (3 patients with pure autonomic failure and 1 patient with
idiopathic Parkinson disease and autonomic dysfunction). After
acarbose was found to be well tolerated during this initial phase, the
remainder of the patients were studied in a double-blind, randomized
fashion. The hospital investigational pharmacy was responsible for
the randomization sequence and kept the blind code. Two identically
Acarbose Attenuates Postprandial Hypotension 55
colored capsules were dispensed each day to maintain the double-
blind nature of the study. All attempts were made to replicate the
experimental conditions between study days.
A 21-gauge catheter was inserted into an antecubital vein for
blood sampling. Blood pressure and HR measurements were ob-
tained with an automated sphygmomanometer attached to the same
arm. Heart rhythm was monitored through ECG leads. Forearm
blood flow was measured using a mercury-in-silastic strain gauge
connected to a plethysmograph (Hokanson EC4, DE; Hokanson Inc)
as described previously.32 A thoracic bioimpedance measurement
device (KIM4; Heinemann and Gregory) was used to calculate
relative changes in cardiac output (CO) and total peripheral resis-
tance (TPR). All of the signals were digitized at a sampling rate of
500 Hz using DI-720USB and Windaq Pro⫹ software (DATAQ
Instruments) and processed with custom software written in PV-
Wave (Visual Numerics Inc).
Subjects remained in the supine position throughout the study to
control for the effect of orthostasis on blood pressure. Premeal
baseline measurements were taken every 5 minutes for 30 minutes.
After this period, the blinded medication was administered by mouth
with 50 mL of plain water. Twenty minutes later, subjects were
asked to ingest a standard solid meal of 423 Kcal (19.9 g of fat,
42.3 g of carbohydrates, and 19.5 proteins) prepared by a certified
nutritionist. The meal was consumed over a 20-minute period. Blood
pressure and HR were monitored every 5 minutes for 90 minutes
after food ingestion.
TPR and Forearm Vascular Resistance
TPR and forearm blood flow were measured at baseline and at 30,
45, 60, and 90 minutes after meal intake. TPR was calculated by
dividing mean arterial pressure (millimeters of mercury) by cardiac
output (milliliters per second) and expressed in peripheral resistance
units. Mean arterial pressure was calculated from the formula
(DBP)⫹1/3(SBP⫺DBP). Forearm vascular resistance (FVR) was
calculated as mean arterial pressure divided by forearm blood flow
and expressed in units of millimeters of mercury milliliters⫺1
deciliters (tissue)⫺1 minutes⫺1.
Hormone Determinations
Catecholamines (norepinephrine and epinephrine), insulin, and glu-
cose levels, were determined at baseline and at 30, 45, 60, and 90
minutes after meal intake through an intravenous catheter placed
ⱖ30 minutes before sampling using assays described previously.33
Statistical Analysis
All of the data are presented as mean⫾SEM. The SBP, DBP, and HR
measurements taken every 5 minutes for 90 minutes after the
intervention (acarbose or placebo) were the primary end points.
Random-effects models were used to examine the difference in time
course between interventions while taking into account the correla-
tion among repeated measurements obtained from individual sub-
jects over time. We also used robust SEs to calculate 95% CIs in
consideration of the small sample size. The baseline SBP and DBP
measurements (the mean of 7 baseline measurements), body mass
index (BMI), linear and quadratic time trend, period, and sequence
were adjusted for as potential confounders.
Secondary end points included a comparison between interven-
tions (acarbose versus placebo) in the following parameters: glucose
and insulin taken at premeal baseline and at 30, 45, 60, and 90
minutes postmeal. Random-effect models were used, and BMI,
period, and sequence were adjusted for as potential confounders.
Tertiary end points included changes in plasma catecholamine
levels, CO, TPR, and FVR. Percentage changes were calculated for
CO and TPR using 4 time points (30, 45, 60, and 90 minutes
postmeal). Differences between interventions at specific time points
were determined using Wilcoxon signed rank test.
All of the tests were 2-tailed, and a P⬍0.05 was considered
significant. Analyses were performed with the SPSS statistical
software (SPSS 14.0, SPSS Inc) or Stata 9.2 (Stata Corp). The
authors had full access to the data and take responsibility for its
56 Hypertension July 2007

TABLE 1. Subjects Clinical Characteristics

Postprandial Fall in Postprandial Increase
No. Diagnosis Gender BMI, kg/m2 Age, y Race SBP/DBP, mm Hg in HR, bpm
1 PD⫹ Female 20.3 66 White ⫺55/–19 7
2 PAF Male 26.1 73 White ⫺48/–19 3
3 PAF Female 21.5 57 White ⫺37/–17 7
4 PAF Female 26.1 57 White ⫺41/–25 5
5 PAF Male 32.5 62 White ⫺23/–3 8
6 PAF Female 25.6 70 White ⫺31/–16 5
7 PAF Female 17.5 71 White ⫺29/–14 8
8 PAF Female 28.6 72 White ⫺24/–9 10
9 PAF Male 25.9 74 White ⫺28/–12 2
10 PAF Male 28.1 45 White ⫺33/–25 4
11 PAF Male 22.7 55 White ⫺32/–23 19
12 PAF Female 22.5 64 White ⫺28/–23 7
13 PAF Female 24.9 79 White ⫺35/–23 2
PAF indicates pure autonomic failure; PD⫹, Parkinson disease with autonomic failure.

integrity. All of the authors have read and agree to the article as pressure on standing without an adequate increase in HR. As
written. expected, supine plasma norepinephrine was low and did not
increase appropriately on standing, consistent with postgan-
Results glionic loss of sympathetic fibers. The decrease in SBP
Basal Cardiovascular and Autonomic Function during phase II of the Valsalva maneuver was exaggerated,
Subjects’ demographic characteristics are presented in Table and the SBP overshoot during phase IV was absent. The
1. All of the subjects fulfilled the diagnostic criteria for PPH; Valsalva ratio was low, indicating inadequate compensatory
the average postprandial fall in SBP and DBP was 34⫾2.6/ changes in HR. The pressor responses to isometric handgrip
17⫾2.2 mm Hg. The postprandial increase in HR was 5⫾1.7 exercise or pain stimulus (cold pressor test) were impaired.
bpm, which is inappropriately low, considering the magni- Sinus arrhythmia was markedly reduced. Hence, autonomic
tude of the postprandial blood pressure fall. testing indicated severe sympathetic and parasympathetic
The results of the autonomic function tests are presented in involvement.
Table 2. All of the patients had a profound decrease in blood
Effect of Acarbose on Hemodynamic and
Neuroendocrine Parameters
TABLE 2. Autonomic Function Tests and Orthostatic Stress
Blood Pressure and HR
Subjects Normal After adjusting for baseline measurements, BMI, period, and
Parameters Enrolled Values* sequence effect, acarbose reduced the postprandial fall in
Orthostatic change in SBP, mm Hg ⫺75⫾7.8 ⱕ20 SBP and DBP by 17 mm Hg (95% CI: 7 to 28; P⫽0.003) and
Orthostatic change in heart rate, bpm 15⫾2.9 5 to 10 9 mm Hg (95% CI: 5 to 14; P⫽0.001), respectively, com-
Supine plasma norepinephrine, pg/mL 110⫾26.6 ⱕ150 pg/mL pared with placebo (Figure 1). HR tended to increase more
during placebo as compared with acarbose, but this effect did
Upright plasma norepinephrine, pg/mL 183⫾60.1 ⬎450 pg/mL
not reach statistical significance; the difference between
SA ratio 1⫾0.02 1.2⫾0.1
acarbose and placebo was ⫺2 bpm (95% CI: ⫺4 to ⫺0.2;
Depressor response to Valsalva during ⫺54⫾8.6 ⱕ20 P⫽0.079; Figure 2). No patients reported any adverse events
phase II, mm Hg
with acarbose.
Pressor response to Valsalva during ⫺30⫾5.2 ⬎20
phase IV, mm Hg† Plasma Catecholamines, Glucose, and Insulin
Valsalva ratio 1.1⫾0.02 1.5⫾0.2 There were no differences in plasma norepinephrine and
Depressor response to hyperventilation, ⫺37⫾5.5 ⫺5⫾6.3 epinephrine postmeal compared with at baseline or between
mm Hg interventions. As expected, acarbose significantly reduced the
Pressor response to cold water hand 9⫾2.2 24⫾13 absorption of glucose by 10 mg/dL (95% CI: 2 to 18;
immersion, mm Hg P⫽0.02) as compared with placebo. Hence, acarbose reduced
Pressor response to handgrip, mm Hg 1⫾3.3 16⫾6 insulin secretion by 11 ␮U/mL (95% CI: 5 to 18; P⫽0.001;
Figure 3) compared with placebo.
SA indicates sinus arrhythmia ratio.
*Normal values are from the Autonomic Dysfunction Center Database at
Because insulin is a known vasodilator, we applied a
Vanderbilt University. statistical model to determine the effect of acarbose on blood
†A negative value for phase IV of the Valsalva maneuver indicates that the pressure after adjusting for plasma insulin levels and other
blood pressure overshoot was absent. confounders (baseline measurements, BMI, period, and se-
 Shibao et al
quence). We found that the total effect of acarbose in
reducing the postprandial fall in SBP decreased from 17 to
14 mm Hg (95% CI: 4 to 25 mm Hg) when the changes in
insulin levels were considered, and the effect of acarbose
remained significant (P⫽0.005). Similarly, the effect on DBP
decreased from 9 to 7 mm Hg (95% CI: 2 to 11 mm Hg;
P⫽0.005). These results indicate that, though insulin may
play a role, there are other factors involved in the attenuation
of PPH by acarbose.
CO, TPR, and FVR
Because of technical difficulties, we were able to obtain
measurements of forearm blood flow and FVR in only 6
patients. CO and TPR were measured in 11 patients. There
were no significant differences in CO between interventions,
Acarbose Attenuates Postprandial Hypotension 57
Figure 1. Change in SBP (circles) and
DBP (squares) measurements during
placebo (open) and acarbose (filled) at
baseline and for 90 minutes postmeal
challenge. Postprandial hypotension was
significantly attenuated with acarbose.
*P⬍0.01.
whereas TPR tended to decrease more with placebo as
compared with acarbose. We found statistical significant
differences at 90 minutes postmeal intake (Figure 4). Further-
more, acarbose significantly attenuated the postprandial de-
crease in FVR compared with placebo. The maximum effect
was observed at 30 minutes postmeal (Figure 5).
Discussion
We found that acarbose effectively attenuates the fall in blood
pressure after meals in patients with severe autonomic failure,
suggesting a potential therapeutic use in the treatment of
PPH. There results are consistent with the hypothesis that
PPH is mediated at least in part by the secretion of vasodi-
latory hormones in response to glucose absorption.
Figure 2. Change in HR measurements
during placebo (‚) and acarbose (Œ)
days at baseline and for 90 minutes
postmeal challenge. The differences
observed between interventions did not
reach statistical significance (P⫽0.08).
58 Hypertension July 2007
The pathophysiology of PPH is complex and likely multi-
factorial. In normal subjects, food ingestion promotes bio-
chemical and hormonal changes, including the secretion of
gastric acid and gut peptides, that result in blood pooling
within the splanchnic circulation.20,34To maintain blood pres-
sure, a variety of hemodynamic changes are necessary,
including an increase in HR, stroke volume, and CO.4 These
responses are partially mediated by a compensatory sympa-
thetic activation as shown by the increase in plasma norepi-
nephrine and muscle sympathetic nerve activity after food
intake in normal subjects.5,34 Failure of these compensatory
mechanisms seems pivotal in the development of PPH,
explaining the greater prevalence of this condition in subjects
with autonomic impairment.
On this background, a few nonpharmacological and phar-
macological interventions have been advocated to prevent the
development of PPH. In mild cases, a reduction in the meal
size or its carbohydrate content may be useful. However, the
latter approach is difficult to adhere to, considering that
Figure 3. A, Changes in plasma glucose during
placebo (E) and acarbose (F) days at premeal
baseline and 30, 45, 60, and 90 minutes post-
meal challenge. B, Change in plasma insulin
during placebo (E) and acarbose (F) days at
premeal baseline and 30, 45, 60, and 90 min-
utes postmeal challenge.
carbohydrates represent 45% to 65% of the normal Western
diet. Severe cases are challenging to treat, and these patients
can be symptomatic even while supine and have a higher risk
of syncope if they stand up after meals. Hence, a pharmaco-
logical intervention is often necessary.
Three different pharmacological approaches have been
used to improve PPH. One approach has been to increase the
baseline sympathetic nervous system with 3,4-DL-threo-
dihydroxyphenylserine before meal ingestion.35 Another has
been to block the release of gastrointestinal and pancreatic
hormones with octreotide.36 A third approach has been to
antagonize the effect of vasodilators, such as adenosine with
caffeine.22 Although these drugs seem to ameliorate PPH,
their use is limited by aspects of their clinical pharmacology,
their mode of application, and adverse effects. For instance,
3,4-DL-threo-dihydroxyphenylserine and other sympathomi-
metics should be taken ⱖ1 hour before meals and may induce
hypertension. Octreotide is expensive, must be administered
subcutaneously, and may induce abdominal cramps or diar-
 Shibao et al
rhea after fatty meals, limiting its use, particularly among
patients with diabetes mellitus. Caffeine has not been found
to be universally effective.37 Thus, it would be advantageous
to develop novel pharmacological interventions for the treat-
ment of PPH.
For this purpose, we studied PPH in patients with severe
peripheral autonomic failure. These subjects suffer from a
neurodegenerative process that affects postganglionic auto-
nomic fibers resulting in low levels of plasma catecholamines
and interruption of the baroreflex arc. By using this patho-
physiological model, we sought to unmask any beneficial
effect of acarbose in PPH.
Considering that, among dietary components, carbohydrate
exerts the greatest hypotensive effects, any slowing of the rate
of carbohydrate absorption could potentially improve PPH.
We used acarbose, a potent competitive inhibitor of intestinal
␣-glucosidase, to delay the absorption of glucose and to
determine its effect on blood pressure after meals. We found
an average improvement of 17 mm Hg after a standard
mixed-meal ingestion in patients with peripheral autonomic
Acarbose Attenuates Postprandial Hypotension 59
Figure 4. A, Percentage of change in CO
during placebo (E) and acarbose (F)
days at 30, 45, 60, and 90 minutes post-
meal challenge. B, Percentage of change
in TPR during placebo (E) and acarbose
(F) days at 30, 45, 60, and 90 minutes
postmeal; *P⬍0.05.
failure. As expected, our patients did not show any sympa-
thetic response to the meal challenge. Plasma norepinephrine
and epinephrine were similar during placebo or acarbose,
indicating that the improvement in blood pressure in our
patients was not explained by sympathetic activation. Con-
versely, acarbose prevented the decrease in TPR and FVR,
supporting the hypothesis that a circulating vasodilator par-
tially suppressed by this drug was mostly responsible for the
fall in blood pressure after meals.
In this context, we argued that insulin could play a role as
a possible mediator of this vascular response. Insulin acts as
a vasodilator via generation of NO,38,39 is normally released
during the postprandial state, and has been shown to decrease
blood pressure when infused intravenously at physiological
levels in patients with autonomic failure.40 In our study, the
attenuation in glucose absorption produced by acarbose
blunted the postprandial peak of insulin, and this coincided
with a reduction in PPH. However, our statistical model
showed that acarbose still had a significant effect in reducing
PPH after adjusting for changes in insulin levels, indicating
60 Hypertension July 2007
that blockade of other vasodilators may contribute to PPH.
These findings are consistent with previous observations that
patients with type 1 diabetes mellitus who, by definition, are
insulin deficient, also develop PPH.24 The action of acarbose
on glucose absorption affects a common pathway that influ-
ences the secretion of other gut hormones with known
vasodilatory actions, such as neurotensin.26,41 It is likely that
more than one vasodilator is involved in the pathophysiology
of PPH.
In conclusion, 100 mg of acarbose taken with meals
effectively attenuates the postprandial decrease in blood
pressure in patients with autonomic failure. Our results
provide a novel therapy for the treatment of this condition.
Perspectives
PPH is commonly associated with syncope, falls, angina, and
cerebrovascular events. Those at most risk are subjects with
varying degrees of autonomic impairment. Effective treat-
ment strategies for this condition are limited. Our study
provides a novel pharmacological approach to treat this
condition; 100 mg of acarbose taken 20 minutes before meals
effectively attenuates the fall in blood pressure induced by
meals in patients with severe autonomic failure. We speculate
that these results can be extrapolated to other patients with
milder forms of autonomic impairment such as the elderly,
but formal studies are needed to evaluate this postulate.
Acknowledgments
We thank the patients with autonomic failure for their contribution to
this research and the nurses of the Clinical Research Center for
their support.
Sources of Funding
This work was supported in part by grants HL56693 and NS055670
and the General Clinical Research Center grant MO1 RR00095. C.S.
was a recipient of the International Fellowship in Clinical Pharma-
cology supported by the Merck Foundation.
Disclosures
None.
Figure 5. Changes in FVR during placebo (E)
and acarbose (F) days at premeal baseline and
30, 45, 60, and 90 minutes postmeal challenge.
The nadir in FVR was observed at 30 minutes
after meal ingestion.
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