Effect of cereal test breakfasts differing in glycemic index and
content of indigestible carbohydrates on daylong glucose tolerance
in healthy subjects1–3
Anne C Nilsson, Elin M Östman, Yvonne Granfeldt, and Inger ME Björck
ABSTRACT
Background: Frequent hyperglycemic episodes are increasingly
being associated with an increased risk of type 2 diabetes and car-
diovascular disease.
Objective: We studied the extent to which acute glycemia and
glycemia after subsequent meals can be modulated by the charac-
teristics of cereal foods, such as glycemic index (GI) and content of
indigestible carbohydrates.
Design: Twelve healthy subjects consumed test meals in a random
order. In series 1, the test meals were consumed at breakfast, and
postprandial blood glucose incremental areas under the curve
(IAUCs) were calculated after the test breakfast, standardized lunch,
and standardized dinner. In series 2, the subjects consumed test
evening meals and IAUCs were calculated after a subsequent stan-
dardized breakfast. Breath hydrogen was measured as an indicator of
colonic fermentation.
Results: Barley or rye kernel breakfasts lowered the blood glucose
IAUC (0 –120 min) at breakfast, at a subsequent lunch, and the
cumulative IAUCs (breakfastѿlunchѿdinner) when compared with
white-wheat bread (P 쏝 0.05). The lunch blood glucose IAUCs were
positively correlated with breakfast IAUCs (r ҃ 0.30, P 쏝 0.05).
Breath hydrogen excretion was negatively correlated with blood
glucose IAUCs after lunch (r ҃ Ҁ0.33, P 쏝 0.05) and dinner (r ҃
Ҁ0.22, P 쏝 0.05). A barley kernel evening meal resulted in lower
IAUCs (P 쏝 0.05) and higher breath hydrogen (P 쏝 0.001) after a
subsequent breakfast compared with white-wheat bread.
Conclusions: Glucose tolerance at subsequent meals can be notably
improved during the course of a whole day or overnight by choosing
specific low-GI, whole-grain cereal products. A low GI may be
sufficient to achieve a second-meal effect from breakfast to lunch. A
specific indigestible carbohydrate mixture appears to be required to
show benefits on glucose tolerance in a longer time frame (9.5 h),
most likely mediated through colonic fermentation. Am J Clin
Nutr 2008;87:645–54.
KEY WORDS GI, glycemic index, indigestible carbohy-
drates, second-meal effect, colonic fermentation, breath hydrogen
INTRODUCTION
An accumulating body of data shows beneficial effects of
low– glycemic index (GI) foods on chronic diseases related to
impairments of glucose and lipid metabolism (1, 2). Epidemio-
logic data suggest that a low-GI diet plays a protective role
against the development of type 2 diabetes (3, 4), coronary artery
Am J Clin Nutr 2008;87:645–54. Printed in USA. © 2008 American Society for Nutrition
disease (1, 5), and the metabolic syndrome (6). Similar preven-
tive effects have also been observed with foods rich in whole
grains (7, 8); therefore, it could be hypothesized that low-GI
foods that are additionally rich in whole-grain constituents could
Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008
be particularly advantageous. The factors underlying the protec-
tive effects of low-GI or whole-grain properties are not fully
clarified but likely include improvements in insulin sensitivity
(6, 9, 10). Recent findings (11–13) suggest that oxidative stress
is a possible mechanism underlying the pathophysiology of di-
abetes and cardiovascular disease. Hyperglycemia, and probably
also elevated concentrations of free fatty acids, induce increased
concentrations of reactive oxygen and nitrogen species (12),
resulting in cell damage, endothelial dysfunction, and vascular
complications (11), as well as ␤-cell dysfunction (14, 15). A
meta-analysis has shown that adults with the metabolic syn-
drome have lower concentrations of several antioxidants (16),
which suggests either a deficiency in dietary supply or that an-
tioxidants have been used to scavenge reactive species emanat-
ing from hyperglycemia. Oxidative stress is likely a key mediator
of increased cytokine concentrations and low-grade systemic
inflammation (17), suggesting its role in the genesis of vascular
damage (18).
Certain low-GI foods can lower glycemia not only in direct
connection to a meal (acutely), but also at a consecutive stan-
dardized second meal, ie, lunch after a test breakfast (19 –22) or
breakfast after a test dinner (23–26), indicating improvements in
insulin sensitivity or insulin economy also within a semi-acute
time frame. In the case of benefits in the breakfast to lunch
scenario, the key factor involved is likely the lente carbohydrate
(ie, carbohydrates capable of maintaining a low but sustained net
increment in blood glucose) features of low-GI foods per se (19,
1
From the Division of Applied Nutrition and Food Chemistry, Depart-
ment of Food Technology, Engineering and Nutrition, Lund University,
Sweden.
2
Supported by European Commission under the Fifth Framework Pro-
gramme of Research and Technical Development QLK1-2001-00431
(EUROSTARCH). The barley and oat kernels were generously provided by
Finax AB, Helsingborg, Sweden, and the wheat and rye kernels by Nord Mills
AB, Malmö, Sweden.
3
Reprints not available. Address correspondence to A Nilsson, Applied
Nutrition and Food Chemistry, Department of Food Technology, Engineer-
ing and Nutrition, Lund University, PO Box 124, SE-221 00 Lund, Sweden.
E-mail: anne.nilsson@inl.lth.se.
Received March 27, 2007.
Accepted for publication October 5, 2007.
645
646 NILSSON ET AL

21, 22). However, in the evening meal to breakfast scenario,
other properties of the low-GI foods, such as the specific amount
or type of indigestible carbohydrates, might contribute to the
improvement in glucose tolerance (24 –26). Colonic fermenta-
tion of indigestible carbohydrates [dietary fiber (DF) and resis-
tant starch (RS)] results in the formation of colonic metabolites,
particularly short-chain fatty acids (mainly acetic, propionic, and
butyric acids) (27, 28). The colonic metabolites may enter the
circulation, and it has been suggested that certain short-chain
fatty acids produced during colonic fermentation may exert sys-
temic effects, including benefits on glucose metabolism (24, 25,
29, 30).
The purpose of the present study was to investigate the effects
of some cereal-based test meals that varied in GI features and
content of indigestible carbohydrates (DF and RS) on acute post-
prandial glucose tolerance as well as on glucose tolerance at
subsequent standardized meals. The postprandial glycemia at
subsequent meals was related to the magnitude of colonic fer-
Malmö, Sweden. The amount of barley DF added to the WWB
meal was intended to correspond to the total DF content naturally
occurring in an equivalent starch portion of boiled barley kernels.
The size of the test meals corresponded to 50 g available starch
(calculated by subtracting RS from total starch). The portion
sizes and contents of available starch, RS, and DF (soluble and
insoluble) are shown in Table 1. The wheat, rye, and barley
kernels were boiled for 30, 35, and 23 min, respectively, in 110
mL water. The oat kernels were boiled for 18 min in 100 mL
water. Salt (0.5 g) was added to the boiling water. All water was
absorbed into the kernels when cooked. The whole-grain barley
flour used for the porridge was suspended in 400 mL water (with
0.5 g salt) and then cooked in a microwave oven for 5 min (600
W) with 2 intermittent breaks for stirring. The products were
served immediately after preparation. The WWB was baked
according to a standardized procedure (31) in a home baking
machine (Severin model no. BM 3983; Severin Svenaka AB,
Djursholm, Sweden). After cooling, the crust was removed and

Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008

mentation of indigestible carbohydrates using breath hydrogen
as an indicator.
SUBJECTS AND METHODS
Meals
Test meals
The test meals included in the study were white-wheat bread
(WWB, reference product), wheat kernels, rye kernels, oat ker-
nels, barley kernels, whole-grain barley flour porridge (made
from flour of the same barley kernels), and WWB enriched with
barley DF (Lyckeby Stärkelsen, Kristianstad, Sweden)
(WWBѿbarley DF). The cereal kernels used were commercially
available, nonspecified Swedish varieties. The barley and oat
kernels were generously provided by Finax AB, Helsingborg,
Sweden, and the wheat and rye kernels by Nord Mills AB,
the bread was sliced and wrapped into aluminum foil in portion
sizes, put into plastic bags, and stored in a freezer. On the day
before the experiment, the bread was removed from the freezer
and thawed at an ambient temperature in its aluminum foil and
plastic bag wrapping. The barley DF extract in the meal with
WWBѿbarley DF was mixed with 250 mL water and consumed
with the WWB. A 250-mL portion of water was served with all
meals.
Standardized meals
In series 1 (test breakfast series), a standardized lunch was
included, consisting of mashed potatoes (Felix Basmos, Procor-
dia Food AB, Eslöv. Sweden) and 100 g meatballs (ICA frozen
meatballs, ICA AB, Solna, Sweden). The meatballs were heated
in a microwave oven according to the manufacturer’s instruc-
tions. The mashed potato powder was mixed with boiled water
(68 g mashed potato powder ѿ 3.5 dL water). A standardized

TABLE 1
Portion sizes and contents of available starch, dietary fiber (DF; soluble and insoluble), and resistant starch (RS) in the test products and meals1

DF

Portion weight2 Available starch3 Insoluble Soluble Total DF RS DF ѿ RS

4
Test products (%)
WWB — 77.1 2.1 1.8 3.9 0.7 4.6
Wheat kernels — 63.1 7.5 2.6 10.1 6.3 16.4
Rye kernels — 61.2 13.1 4.4 17.5 4.6 22.1
Oat kernels — 58.8 6.4 2.9 9.3 4.7 14.0
Barley kernels — 59.3 7.3 3.4 10.7 9.5 20.2
Barley DF — 21.9 30.2 30.4 60.6 0.4 61.0
Barley porridge — 71.3 9.4 3.7 13.1 2.4 15.5
Test meals (g/serving)
WWB 118.9 50 2.3 2.0 4.3 0.8 5.1
Wheat kernels 90.5 50 5.9 2.1 8.0 5.0 13.0
Rye kernels 93.0 50 10.6 3.6 14.2 3.7 17.9
Oat kernels 118.9 50 5.4 2.5 7.9 4.0 11.9
Barley kernels 95.5 50 6.2 2.9 9.1 8.0 17.1
White WB ѿ barley DF 95.3 50 6.6 6.3 12.9 0.8 13.7
Barley porridge 115.5 ѿ 15.8 50 6.6 2.6 9.2 1.7 10.9
1
WWB, white wheat bread (reference product).
2
The portion weight of the white WB was measured as eaten. Cereal kernels, barley DF, and barley flour were ambient dry and uncooked.
3
Available starch calculated by difference between total starch (33) and RS (34).
4
Values are presented as % of dry matter.
 PROLONGED IMPROVED GLUCOSE TOLERANCE
WWB (122.9 g fresh weight, Jätterasken, Pågen AB, Malmö,
Sweden), with the crust removed, was included as a standardized
dinner. The WWB and mashed potato portions were equivalent
to 50 g available starch (32). At 2 h after commencing the test
breakfast and the standardized lunch, respectively, the partici-
pants were served 150 mL water and 150 mL coffee or tea
without milk or sugar (individually standardized to the subjects).
In series 2 (test evening meal series), a standardized breakfast
was provided that was identical in content to the standardized
dinner in the test breakfast series. Water (250 mL) was consumed
with all meals.
Analysis of total starch, resistant starch, and dietary
fiber in the test products
The test products were analyzed with respect to total starch
(33), RS (34), and DF (soluble and insoluble) (35). To analyze
total starch and DF, the cereal kernels were boiled, air dried, and
milled (Cyclotec, Foss Tecator AB, Höganäs, Sweden); the
WWB was air dried and milled; and the whole-grain barley
porridge was analyzed in the same form as when it was con-
sumed. To analyze RS, all test products were analyzed in the
same form as when eaten. Available starch was calculated by
subtracting RS from total starch.
Experimental design
Test subjects and procedure
Twelve healthy subjects (5 women and 7 men) aged 21– 41 y
(mean 앐 SD ҃ 28.3 앐 5.1 y) and with normal body mass indexes
(mean 앐 SD: 22.1 앐 2.0, in kg/m2) participated in the study.
Approval of the study was given by the Regional Ethical Review
Board in Lund, Sweden. The subjects were encouraged to stan-
dardize their meal patterns and to avoid foods rich in DF the day
before an experimental day. Furthermore, they were asked to
avoid alcohol and excessive physical exercise in the evening or
morning before an experiment. Finally, they were not to have
consumed antibiotics or probiotics for 2 wk before the experi-
ment. The test meals were consumed in a random order.
In series 1 (test breakfast series; Figure 1), the test meals
included were WWB, wheat kernels, barley kernels, oat kernels,
rye kernels, whole-grain barley flour porridge, and WWBѿ
barley DF. Each subject participated at 7 occasions, once or twice
a week, with each occasion being 욷3 d apart. At 2030 in the
evening before the experimental days, the subjects consumed an
individually standardized evening meal composed of WWB and
water. After this meal, they were fasting for 앒10 h until breakfast
the next morning. On the experimental days, the subjects arrived
at 0745 and sat resting until 0800. At that point, fasting blood
FIGURE 1. Experimental design of series 1.
647
FIGURE 2. Experimental design of series 2.
glucose and breath hydrogen were measured, and subsequently
one of the cereal test meals was served. The postprandial blood
glucose concentration was measured repeatedly during a 2-h
period after the start of the test breakfast, standardized lunch
(served at 1200), and standardized dinner (served at 1730), re-
spectively. Breath hydrogen was measured every half-hour dur-
ing the 11.5 h after the cereal test meals. Coffee or tea and water
were served 2 h after the start of the breakfast and lunch, respec-
Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008
tively. The subjects were told to maintain a low but consistent
level of physical activity throughout the experimental day.
In series 2 (test evening meal series; Figure 2), the test meals
were consumed as late evening meals at 2230 in a random order,
once or twice a week and at least 3 days apart. The time point for
the evening meal was chosen to achieve the same time interval
between the test meal and breakfast in series 2 as between the test
breakfast and evening meal in series 1. The test evening meal
consisted of either WWB, barley kernels, or WWBѿbarley DF.
On the subsequent morning, the subjects consumed a standard-
ized WWB breakfast. Each subject participated once or twice a
week at 3 separate occasions. Blood glucose and breath hydrogen
were determined at fasting and repeatedly during the 2-h period
after the standardized breakfast. In all other respects, the proce-
dure was similar to that of series 1.
Sampling and analyses of blood glucose and hydrogen
in expired air
To measure the blood glucose concentration, finger-prick cap-
illary blood samples (HemoCueB-glucose; HemoCue AB, Án-
gelholm, Sweden) were taken before the breakfast, lunch, and
evening meals and again at 15, 30, 45, 60, 90, and 120 min in the
postprandial phase of the respective meals. The blood glucose
concentration before each meal (time ҃ 0) was used as the basal
value in the statistical calculations. Breath hydrogen was mea-
sured as a marker of colonic fermentation, and was measured at
fasting and at half-hour increments during the experimental day
with an EC 60 gastrolyzer (Bedfont EC60 Gastrolyzer, Roches-
ter, England). In series 1, the statistical calculations were based
on breath hydrogen samples taken 4 h after the breakfast.
Calculations and statistical methods
The GIs of the test products were determined after the break-
fast test meals. GIs and glucose areas were determined by using
the 0 –120-min incremental blood glucose areas under the curves
(IAUCs), ignoring the negative areas. The GIs were calculated as
the mean of individual ratios (36). GraphPad Prism (version 4.03;
GraphPad Software, San Diego, CA, USA) was used for graph
plotting and calculating glucose IAUCs. WWB was used as a
reference product in the GI calculations. Significant differences
among glucose IAUCs and breath hydrogen means were deter-
mined with analysis of variance (ANOVA general linear model)
648 NILSSON ET AL

followed by Tukey’s multiple-comparison test (MINITAB Sta- TABLE 2

tistical Software, release 13.32 for WINDOWS; Minitab Inc, Blood glucose concentrations before each meal after different test
State College, PA). Participants acted as their own control. breakfasts and mean blood glucose concentrations before the breakfast,
lunch, and dinner meals1
With the exception of postprandial blood glucose concentra-
tions after the standardized meals in test series 1 and in test series Glucose concentrations before the meals
2, the differences in test parameters in a series of time points were
analyzed by using a mixed model (PROC MIXED in SAS release Breakfast
8.01; SAS Institute Inc, Cary, NC) with repeated measures and an Test breakfast meals (fasting) Lunch Dinner
autoregressive covariance structure. When significant interac- mmol/L
tions between treatment (ie, test meals) and time were found,
WWB 4.7 앐 0.1a 4.2 앐 0.2a 3.9 앐 0.2a,b
Tukey’s tests were performed at each instance (MINITAB, re- Barley porridge 4.8 앐 0.1a 4.4 앐 0.1a,b 4.0 앐 0.1a,b
lease 13.32; Minitab Inc). The blood glucose concentrations be- Wheat kernels 4.5 앐 0.1a 4.5 앐 0.1a,b 4.0 앐 0.1a,b
fore and after the standardized meals in test series 1 and in test Oat kernels 4.6 앐 0.1a 4.4 앐 0.1a,b 3.8 앐 0.1a
series 2 were dependent on the preceding test meals. To achieve Rye kernels 4.6 앐 0.1a 4.3 앐 0.1a,b 3.9 앐 0.1a,b
a measure of the incremental blood glucose response after the Barley kernels 4.7 앐 0.1a 4.7 앐 0.1b 4.3 앐 0.1b
standardized meals with basal values immediately before the White WB ѿ barley DF 4.6 앐 0.1a 4.3 앐 0.1a,b 4.0 앐 0.1a,b
meals set to 0 mmol/L, analyses were performed with ANOVA Mean blood glucose 4.6 앐 0.0A 4.4 앐 0.1B 4.0 앐 0.1C
followed by Tukey’s test at the specific test points. concentrations

Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008

Spearman’s rank correlation was used to study relations be-
tween test variables. A correlation for each subject was calcu-
lated, and from these values the mean value of Spearman’s cor-
relation coefficient was obtained. To determine the P value, a
permutation test was performed by using MATLAB with the null
hypothesis that no correlations existed (the alternative hypothe-
sis was that the data were correlated). The results are expressed
as means 앐 SEMs. Values P ⱕ 0.05 were considered statistically
significant throughout the study.
RESULTS
Series 1 (test breakfast series): course of the day
perspective
Effects of different cereal test products consumed at
breakfast on postprandial blood glucose increments after the
breakfast, a standardized lunch, and a standardized dinner
An overview of the postprandial blood glucose increments
during the course of the experimental day (test breakfast, stan-
dardized lunch, and standardized dinner) is shown in Figure 3.
FIGURE 3. A significant effect of time (P 쏝 0.0001) and a significant
treatment ҂ time interaction (P 쏝 0.0001) were found on basal blood glucose
concentrations throughout the test day (n ҃ 12 healthy subjects). WWB,
white-wheat bread; DF, dietary fiber.
1
All values are x៮ 앐 SEM; n ҃ 12 healthy subjects. WWB, white-wheat
bread; DF, dietary fiber. A significant effect of time (P 쏝 0.0001) and a
significant treatment ҂ time interaction were found (P 쏝 0.0001). Values in
a column not sharing the same lowercase letter are significantly different, and
values in a row not sharing the same capital letter are significantly different,
P 쏝 0.05 (Tukey’s test).
The mean baseline blood glucose concentrations showed a ten-
dency to decrease during the course of the experimental day.
Accordingly, when we investigated the blood glucose concen-
trations immediately before the meals (time ҃ 0 at breakfast,
lunch, and dinner, respectively), a significant effect of time (P 쏝
0.0001) was found throughout the test day as well as a significant
treatment ҂ time interaction (P 쏝 0.0001). The mean blood
glucose concentrations before the lunch and dinner meals were
lower than the mean fasting glucose concentrations before break-
fast (P 쏝 0.001 and P 쏝 0.0001, respectively). The mean glucose
concentration before dinner was also lower than the correspond-
ing value before lunch (P 쏝 0.0001; Table 2). There were no
significant differences in fasting blood glucose concentrations
before the start of the test breakfasts. However, before the stan-
dardized lunch, the barley kernel breakfast resulted in signifi-
cantly higher glucose concentrations than did the WWB break-
fast (P 쏝 0.05; Table 2). Furthermore, before the standardized
dinner meal, blood glucose concentrations were higher after the
barley kernel breakfast than after the breakfast of boiled oat
kernels (P 쏝 0.05).
The boiled barley and rye kernel breakfasts resulted in lower
GIs than did the breakfast composed of WWB (P 쏝 0.001 and P
쏝 0.01, respectively; Table 3) or whole-grain barley porridge (P
쏝 0.01 and P 쏝 0.05, respectively). In addition, the early post-
prandial glucose response (IAUC 0 – 60 min) was lower (Ҁ33%)
after the WWBѿbarley DF test breakfast than after the WWB (P
쏝 0.05).
When the blood glucose responses after the breakfast, lunch,
and dinner meals were expressed as mean IAUCs (0 –120 min),
a significant effect was found of treatment along the test day (P
쏝 0.001), whereas no treatment ҂ time interaction was observed
(Table 3). The blood glucose increments during the whole test
day, as measured with IAUCs 0 –120 min after the breakfast,
lunch, and dinner, were significantly lower after the barley kernel
or the rye kernel breakfasts than after the WWB breakfast (P 쏝
0.001 and P 쏝 0.05, respectively). The blood glucose IAUCs
 PROLONGED IMPROVED GLUCOSE TOLERANCE 649
TABLE 3
Glycemic index (GI) characteristics and postprandial blood glucose incremental areas under the curve (IAUCs; 0 –120 min) after the test breakfast and the
following standardized lunch and standardized dinner, respectively, and also the total blood glucose IAUCs (breakfast ѿ lunch ѿ dinner) after the
different test breakfasts1
IAUC (0 –120 min)

Test meal GI Breakfast Lunch Dinner Total2

% mmol 䡠 min/L
WWB 100 a
145.4 앐 22.4 192.5 앐 28.9 360.6 앐 36.3 698.5 앐 70.7a
Barley porridge 112 앐 25a 134.6 앐 20.6 157.0 앐 17.8 366.9 앐 23.9 658.5 앐 41.8a,b
WWB ѿ barley DF 93 앐 15a,b 116.0 앐 14.8 156.2 앐 21.9 379.7 앐 17.6 651.9 앐 42.0a,b
Oat kernels 85 앐 13a,b 105.0 앐 15.1 137.1 앐 17.0 372.6 앐 34.7 614.7 앐 49.3a,b,c
Wheat kernels 79 앐 13a,b 100.4 앐 17.5 127.4 앐 14.2 361.0 앐 33.5 588.8 앐 40.5a,b,c
Rye kernels 73 앐 19b 80.6 앐 11.3 130.7 앐 21.2 345.8 앐 36.0 557.1 앐 58.2b,c
Barley kernels 49 앐 7b 68.2 앐 11.8 107.7 앐 14.4 309.6 앐 25.6 485.5 앐 40.1c
1
All values are x៮ 앐 SEM; n ҃ 12 healthy subjects. WWB, white-wheat bread; DF, dietary fiber. Significant effects of treatment (type of breakfast) (P 쏝
0.001) and of time (P 쏝 0.0001) were found along the test day, whereas no treatment ҂ time interaction was seen. Means in a column not sharing the same
superscript letter are significantly different, P 쏝 0.05 (ANOVA followed by Tukey’s test).

Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008

2
The combined blood glucose IAUCs after the breakfast, lunch, and dinner.

during the test day were also lower after the barley kernel break-
fast than after the breakfasts consisting of whole-grain barley
porridge or WWBѿbarley DF (P 쏝 0.01). In addition, a signif-
icant effect of time on blood glucose IAUCs (0 –120 min) was
seen throughout the test day; that is, the blood glucose IAUCs
increased significantly during the day (P 쏝 0.0001). Conse-
quently, the mean blood glucose IAUCs (0 –120 min) after the
dinner (356.6 앐 11.3 mmol 䡠 min/L) were significantly larger (P
쏝 0.0001) than both the mean blood glucose IAUCs after break-
fast (107.7 앐 6.7 mmol 䡠 min/L) and those after lunch (144.1 앐
7.8). The blood glucose IAUCs after lunch were also signifi-
cantly higher than those after the breakfast (P 쏝 0.01).
A significant treatment effect (P 쏝 0.0001) and a significant
interaction (treatment ҂ time, P 쏝 0.001) were found after the
breakfast meal (0 –120 min) (Figure 4). The lowest postprandial
blood glucose increments were achieved after a barley or rye
FIGURE 4. Mean acute incremental blood glucose changes (⌬) after the
different cereal breakfasts. A significant treatment (type of breakfast) effect
(P 쏝 0.001) and a significant interaction (treatment ҂ time, P 쏝 0.0001) were
found over the test period. At a given point in time, values not sharing the
same letters are significantly different, P 쏝 0.05 (ANOVA followed by
Tukey’s test). n ҃ 12 healthy subjects. WWB, white-wheat bread; DF,
dietary fiber.
kernel breakfast. The barley or rye kernel breakfasts resulted in
significantly lower blood glucose peaks (1.5 앐 0.2 mmol/L and
1.6 앐 0.2 mmol/L, respectively, based on individual peak incre-
ment) than did breakfasts of WWB (3.2 앐 0.4 mmol/L; P 쏝
0.0001), whole-grain barley porridge (2.9 앐 0.3 mmol/L, barley/
rye; P 쏝 0.001 and P 쏝 0.01, respectively), or oat kernels (2.7 앐
0.2 mmol/L, barley/rye; P 쏝 0.01 and P 쏝 0.05, respectively).
The breakfast consisting of whole-grain barley flour porridge
resulted in the fastest rise in blood glucose concentration after
breakfast. Consequently, the blood glucose increment at 15 min
was significantly higher after the whole-grain barley porridge
breakfast than after a breakfast of boiled barley kernels or
WWBѿbarley DF (P 쏝 0.01). The breakfast with WWBѿbarley
DF showed a delay in the mean blood glucose peak (Figure 4).
Moreover, the drop in blood glucose concentrations in the later
postprandial phase (90 –120 min after the breakfast) was less
steep after the consumption of WWBѿbarley DF. Consequently,
the blood glucose increment remained higher at 120 min after the
WWBѿbarley DF breakfast than after the WWB, barley kernel,
and barley porridge (P 쏝 0.05).
In the postprandial period after the standardized lunch with the
highest blood glucose increments, that is, 30 – 60 min after the
standardized lunch, a breakfast of barley kernels resulted in sig-
nificantly lower blood glucose increments than did the WWB (30
min, P 쏝 0.001; 45 min, P 쏝 0.05; 60 min, P ҃ 0.001) (Figure
5). At 30 min after the start of the standardized lunch, a barley
kernel breakfast also resulted in lower blood glucose increments
than did breakfasts consisting of whole-grain barley porridge or
WWBѿbarley DF (P 쏝 0.05). At 60 min after the start of the
lunch, all the kernel-based breakfasts resulted in lower blood
glucose increments than did a breakfast of WWB (P 쏝 0.05). The
blood glucose IAUCs (0 –120 min) after the standardized lunch
were positively correlated with the blood glucose IAUCs (0 –120
min) after the cereal test breakfast (r ҃ 0.30, P 쏝 0.05).
No significant effects of the type of breakfast consumed were
seen after the standardized dinner meals, at 9.5–11.5 h after the
test breakfasts (Figure 6). However, the cumulative postprandial
glucose IAUCs (0 –120 min) over the entire test period (breakfast
ѿ lunch ѿ dinner) were significantly lower after the barley
kernel or the rye kernel breakfasts than after the WWB breakfast
650 NILSSON ET AL
FIGURE 5. Mean blood glucose incremental changes (⌬) after a stan-
dardized lunch, 4 h after different cereal test breakfasts. At a given point in
time, values not sharing the same letter are significantly different, P 쏝 0.05
(ANOVA followed by Tukey’s test). n ҃ 12 healthy subjects. WWB, white-
wheat bread; DF, dietary fiber.
(Figure 7). The cumulative glucose IAUCs (breakfast ѿ lunch
ѿ dinner) after the barley kernel breakfast were also lower than
after breakfasts consisting of whole-grain barley porridge or
WWBѿbarley DF, respectively. The cumulative postprandial
glucose IAUCs after the breakfast (0 –120 min) and lunch (0 –
120 min) were lower after all kernel-based breakfasts than after
the WWB breakfast (barley, P 쏝 0.0001; rye, P 쏝 0.001; wheat,
P 쏝 0.01; oat, P 쏝 0.05, respectively). In addition, the barley
kernel breakfast resulted in lower cumulative blood glucose
IAUCs (breakfast ѿ lunch) than did whole-grain barley porridge
(P 쏝 0.01) or WWBѿbarley DF (P 쏝 0.05). The blood glucose
IAUCs (0 –120 min) at the standardized lunch and dinner meals
were inversely correlated to the blood glucose value before the
start of the meals (r ҃ Ҁ0.64, P 쏝 0.001, and r ҃ Ҁ0.39, P 쏝
0.01, respectively).
Breath hydrogen excretion
The mean breath hydrogen excretions after the different test
breakfasts (at lunch, dinner, and total) are shown in Figure 8.
With respect to mean breath hydrogen excretion at lunch and
FIGURE 6. Mean blood glucose incremental changes (⌬) after a stan-
dardized dinner, 9.5 h after different cereal test breakfasts. No significant
effects of breakfast were found over the test period. n ҃ 12 healthy subjects.
WWB, white-wheat bread; DF, dietary fiber.
FIGURE 7. Cumulative glucose incremental areas under the curve (0 –
120 min) at breakfast (B), lunch (L), and dinner (D), respectively. Bars in a
group not sharing the same letter, have different cumulative areas, P 쏝 0.05
(ANOVA followed by Tukey’s test). n ҃ 12 healthy subjects. WWB, white-
Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008
wheat bread; DF, dietary fiber.
dinner, significant effects of product (P 쏝 0.0001) and time (P 쏝
0.05) were found, as well as a significant treatment ҂ time
interaction (P 쏝 0.001; Table 4). At the standardized lunch, 4 – 6
h after the test breakfast, the mean breath hydrogen excretion was
higher after the rye kernel breakfast than after all the other break-
fasts except for the barley kernel breakfast. The barley kernel
breakfast resulted in higher mean breath hydrogen excretion at
lunch in comparison with WWB, and after the standardized din-
ner (9.5–11.5 h), barley kernels resulted in higher mean hydrogen
excretion compared with all other breakfast meals except for oat
kernels. The mean hydrogen excretion at dinner was higher after
the oat kernel breakfast than after the WWB and whole-grain
barley porridge breakfasts. Breath hydrogen excretion at the
standardized lunch and dinner meals was negatively correlated to
the blood glucose IAUCs (0 –120 min) at the same meals (lunch,
r ҃ Ҁ0.33, P 쏝 0.05; dinner, r ҃ Ҁ0.22, P 쏝 0.05).
FIGURE 8. Overview of breath hydrogen concentrations during the
course of the experimental day, after different cereal test breakfasts. n ҃ 12
healthy subjects. WWB, white-wheat bread; DF, dietary fiber.
 PROLONGED IMPROVED GLUCOSE TOLERANCE 651
TABLE 4 the barley kernel evening meal and the evening meal of
Mean breath hydrogen concentrations during 2 h after the standardized WWBѿbarley DF (115.5 앐 15.6 mmol 䡠 min/L). In contrast,
lunch (4 – 6 h) and dinner meals (9.5–11.5 h), respectively, and mean when examining the 0 –90-min blood glucose IAUCs, the barley
hydrogen concentrations (4 –11.5 h) after consuming the different cereal
kernel evening meal induced a lower area at breakfast (72.4 앐
test breakfasts1
10.2 mmol 䡠 min/L) than did either the WWB or WWBѿbarley
Breath hydrogen excretion DF meals (110.5 앐 9.4 and 104.9 앐 12.6 mmol 䡠 min/L, respec-
tively; P 쏝 0.05). Fasting blood glucose concentrations were
Lunch Dinner Total lower after the evening meal of WWB (4.38 앐 0.11 mmol/L) than
Test meals (4 – 6 h) (9.5–11.5 h) (4 –11.5 h) after those of barley kernels (4.73 앐 0.12 mmol/L, P ҃ 0.05) or
ppm WWBѿbarley DF (4.77 앐 0.12 mmol/L, P 쏝 0.05).
WWB 18.0 앐 3.6 a
22.9 앐 3.1a 17.2 앐 2.6a
Barley porridge 28.6 앐 4.9a,b 26.1 앐 3.2a 25.0 앐 3.5a,b Breath hydrogen excretion after the standardized breakfast
Wheat kernels 28.7 앐 5.1a,b 33.8 앐 6.0a,b 29.9 앐 5.5a,b,c The mean breath hydrogen concentration after the standard-
Oat kernels 31.7 앐 5.6a,b 42.7 앐 4.2b,c 36.4 앐 4.4b,c,d
ized breakfast (0 –120 min) was significantly higher after an
Rye kernels 52.6 앐 8.4c 37.2 앐 4.6a,b 41.0 앐 5.1c,d
evening meal of barley kernels than after an evening meal of
Barley kernels 39.3 앐 7.6b,c 52.7 앐 6.8c 46.3 앐 6.5d
WWB ѿ barley DF 27.1 앐 4.1a,b 36.4 앐 4.0a,b 31.7 앐 4.1b,c WWB (54.9 앐 9.9 and 18.4 앐 2.9 ppm, respectively; Figure 10)
(P 쏝 0.001). There were no significant differences (P ҃ 0.09) in
1
All values are x៮ 앐 SEM; n ҃ 12 healthy subjects. WWB, white-wheat mean breath hydrogen concentrations in the morning after an

Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008

bread; DF, dietary fiber. Significant effects of product (P 쏝 0.0001) and of
evening meal of barley kernels compared with WWBѿbarley
time (P 쏝 0.05) and a significant treatment ҂ time interaction were found (P
DF (37.4 앐 6.8 ppm), and no significant differences (P ҃ 0.06)
울 0.001). Values in a column not sharing the same superscript letter are
significantly different, P 쏝 0.05 (ANOVA followed by Tukey’s test). were obtained in mean hydrogen excretion at breakfast after the
evening meal of WWBѿbarley DF compared with WWB.

Series 2 (test evening meal series): overnight perspective
Postprandial blood glucose increments after a standardized
breakfast after different cereal-based evening meals
A significant treatment effect of the preceding evening test
meal was noted in blood glucose increments in the 45– 60-min
postprandial period after the standardized breakfast (Figure 9).
At 45 min after the start of the standardized breakfast, the blood
glucose increment was significantly lower after an evening meal
with barley kernels than after both an evening meal of WWB (P
쏝 0.01) and of WWBѿbarley DF (P 쏝 0.05). When expressed
as IAUCs (0 –120 min), the postprandial blood glucose response
after the standardized breakfast was lower after an evening meal
of barley kernels than after a corresponding evening meal of
WWB (IAUCs of 80.9 앐 12.4 and 121.6 앐 10.7 mmol 䡠 min/L,
respectively; P 쏝 0.05). There were no significant differences (P
҃ 0.06) in the 0 –120-min blood glucose IAUCs at breakfast after
Comparisons between series 1 and series 2
The blood glucose response (0 –120 min IAUCs) at a stan-
dardized WWB meal was significantly higher at 9.5 h after the
test breakfasts than the corresponding area obtained at 9.5 h after
the various test evening meals (Figure 11). That is, the blood
glucose response was higher in the evening than in the morning
(P 쏝 0.0001). There were, however, no corresponding differ-
ences in mean hydrogen concentrations at 9.5–11.5 h after the
test meals depending on whether the test period was from
evening meal to breakfast or from breakfast to evening meal
(Figure 12).

FIGURE 9. Mean blood glucose incremental changes (⌬) after a stan-
dardized breakfast, 9.5–11.5 h after different test evening meals. At a given
point in time, values not sharing the same letter are significantly different, P
쏝 0.05 (ANOVA followed by Tukey’s test). n ҃ 12 healthy subjects. WWB,
white-wheat bread; DF, dietary fiber.
FIGURE 10. Mean breath hydrogen concentrations after a standardized
breakfast, 9.5 h after different test evening meals. A significant treatment
(type of breakfast) effect (P 쏝 0.001, Tukey’s test) was found, whereas no
treatment ҂ time interaction was seen along the test period. n ҃ 12 healthy
subjects. WWB, white-wheat bread; DF, dietary fiber.
652 NILSSON ET AL
FIGURE 11. Blood glucose responses to a standardized meal consumed
9.5 h after test meals consumed either at dinner (filled symbols) or at breakfast
(open symbols). The blood glucose responses to all test meals were higher
9.5 h after a breakfast compared with 9.5 h after an evening meal, P 쏝 0.0001
(ANOVA followed by Tukey’s test). n ҃ 12 healthy subjects. WWB, white-
wheat bread; DF, dietary fiber.
DISCUSSION
The lack of difference in acute glycemic area after breakfasts
consisting of whole-grain barley flour porridge compared with
the WWB make us conclude that the low-GI features observed in
the present work with barley kernels are probably not related to
the amounts of cereal DF present in barley kernels per se. This
supports previous observations (37–39) showing that disruption
of the botanical structure of cereal kernels before heat treatment,
for example, by grinding to a whole-grain flour, renders the
starch highly susceptible to digestive enzymes. The barley DF
used in the WWBѿbarley DF meal contained a substantial frac-
tion of soluble DF (28% dry weight basis), which was made up
almost exclusively of ␤-glucans, yielding 앒4 g ␤-glucans/serv-
ing. The beneficial effect of ␤-glucans on the acute glucose
response in the present study (IAUC 0 – 60 min) is in line with
previous studies with oat ␤-glucans, showing that 4 g ␤-glucans
seems to be a critical amount to elicit a significant decrease in
glucose response to a breakfast based on ␤-glucan-enriched
muesli served with yogurt and WWB (40). Clearly, ␤-glucans
from oats and barley appear to have similar benefits on acute
glycemia. The lack of effect of WWBѿbarley DF when calcu-
lating the 0 –120-min blood glucose IAUCs was due to a higher
blood glucose increment in the later (60 –120 min) postprandial
phase. A prolonged net increment in blood glucose concentra-
tions in the late postprandial phase was observed also after en-
richment of the meal with 4 g oat ␤-glucans (40) and can be
considered beneficial in that a hypoglycemic state in between
meals is avoided. The low-GI features of barley and rye kernels
in the present study are consistent with previous observations, as
are the findings in the present work of high-GI features of whole-
grain barley flour and boiled oat kernels (37).
In the present study, the glycemic response to the breakfast
products seemed to be an important factor in predicting the glu-
cose response at the subsequent lunch. Consequently, a signifi-
cant positive correlation was observed between the blood glu-
cose responses (IAUCs 0 –120 min) after the test breakfasts and
the glucose responses (IAUCs 0 –120 min) after the subsequent
standardized lunch. This finding agrees with previous studies
showing that a low-GI breakfast with lente carbohydrates may
significantly reduce postprandial glycemia after a standardized
lunch meal (19, 21, 22), independent of the content of indigest-
ible carbohydrates. However, although the low-GI feature per se
probably is the most important factor for the benefits on glucose
tolerance seen in a shorter in-between meal period (from break-
fast to lunch), additional mechanisms deriving from colonic fer-
mentation cannot be excluded in the case of rapidly fermentable
carbohydrates, such as lactulose (41). In the present study of
using breath hydrogen excretion as an indicator, signs of colonic
fermentation were seen already at the time of the lunch meal,
especially after the rye kernel breakfast. However, the conclusive
results from previous studies and the positive correlation be-
tween glycemia at breakfast and glycemia at lunch in the present
study make us conclude that the glycemic features of a cereal-
based breakfast are the major determinant of glycemia at the
subsequent lunch.
Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008
The cumulative glycemic response (IAUCs of breakfast ѿ
lunch ѿ dinner) was highly positively correlated to the GI of the
breakfast product (r ҃ 0.63, P 쏝 0.001). Nevertheless, no sig-
nificant correlation was seen between the glucose IAUCs after
breakfast and after the standardized dinner (r ҃ 0.16, P ҃ 0.18)
(test breakfast series). Previous studies have shown that a low-GI
spaghetti evening meal has no effect on the glucose tolerance at
a standardized breakfast consumed 10.5 h later (25, 26), whereas
boiled barley kernels significantly lower the glucose response.
This indicates that in a longer time perspective, eg, from break-
fast to the evening meal, the GI of the food per se is probably not
effective. The fact that a significant negative correlation between
breath hydrogen excretion and glucose response was observed at
the standardized dinner supports previous suggestions of an im-
portant additional effect on glucose tolerance mediated by me-
tabolites produced during colonic fermentation of specific indi-
gestible carbohydrates (24, 25) at that point. Considering the lack
of effect of whole-grain barley porridge or WWBѿbarley DF in
FIGURE 12. Breath hydrogen concentrations after a standardized meal
consumed 9.5 h after test meals consumed either at dinner (filled symbols) or
at breakfast (empty symbols). There were no significant differences depend-
ing on when the test meals were consumed (breakfast or dinner). n ҃ 12
healthy subjects. WWB, white-wheat bread; DF, dietary fiber.
 PROLONGED IMPROVED GLUCOSE TOLERANCE
the lowering of the cumulative glucose IAUCs, it can be sug-
gested that the intact structure and the concomitant elevation in
content of RS in the barley and rye kernels may have contributed
to the effect. It was previously shown that intake of RS, 30 g/d for
4 wk, or 60 g RS the day before the test day (type 2 RS), improves
insulin sensitivity in healthy subjects (42, 43).
In series 2, the time period in between the test evening meal
and the standardized breakfast was 9.5 h and thus similar to the
time interval between the test breakfast and the standardized
dinner in series 1. When comparing the glucose IAUCs 9.5 h after
the test meals in series 1 and series 2, the glucose areas were
larger after the standardized WWB dinner (series 1) than after the
corresponding standardized WWB breakfast (series 2). This in-
dicates a lower glucose tolerance in the evening than in the
morning. The decrease in glucose tolerance seen in healthy sub-
jects over the course of the day was reported previously (44, 45)
and is the opposite of what could be expected in diabetic (type 2
diabetes and type 1 diabetes) or obese subjects (44). More knowl-
edge about potential differences in glucose tolerance during the
course of a day is of importance and may have implications for
diagnosis based on oral-glucose-tolerance tests and measure-
ment of GI, to name a few. In the present study, the baseline
glucose concentrations before the meals dropped from breakfast
to lunch and dropped again from lunch to dinner. The drop was,
however, less pronounced after the barley kernel breakfast,
which might be associated with benefits on insulin sensitivity
through a mechanism related to a prolonged suppression of free
fatty acid concentrations in the blood. This proposal could be
strengthen by the negative correlations observed between blood
glucose IAUCs (0 –120 min) and the basal blood glucose con-
centrations before the lunch and dinner meals, respectively. It
was previously reported that fasting glucose concentrations,
when measured repeatedly during daytime, decline from the
morning to the evening in healthy subjects (44, 46). It should be
noted that the total caloric intake during the experimental days in
this study was between 1000 and 1060 kcal per person and con-
sequently lower than the recommended daily caloric intake for
most healthy adults.
Prospective studies that include a large number of subjects
have indicated that dietary supplementation with acarbose, an
␣-glucosidase inhibitor, importantly delays the onset of type 2
diabetes (47) and reduces the risk of cardiovascular disease and
hypertension (48) in glucose-intolerant subjects. The beneficial
effect of acarbose is proposed to derive from a reduced oxidative
stress and subclinical inflammation due to lower postprandial
glucose excursion (47, 49). The effect of acarbose is thus similar
to that of starchy foods with a low GI. It could therefore be
hypothesized that a low-GI diet, by virtue of maintaining tighter
blood glucose regulation, decreases oxidative stress and low-
grade inflammation. Acute hyperglycemia also induces in-
creased concentrations of circulating cytokines (tumor necrosis
factor-␣, interleukin-6, interleukin-18) in healthy subjects (17).
Low-grade inflammation in healthy subjects has been connected
to an adverse effect on insulin sensitivity, glucose and lipid
metabolism, and blood pressure (50). In particular, frequent post-
prandial hyperglycemic episodes appear to be more prone to
initiate cytokine production (17), indicating that tight glucose
regulation may protect against cardiovascular disease (51). Con-
sequently, low-GI foods capable of reducing blood glucose ex-
cursions during the course of a whole day, or in an overnight
perspective, could be expected to further add to the beneficial
653
effects of low-GI diets. As judged from the present work, low-GI
cereals rich in fermentable carbohydrates might be advantageous
in this respect. In previous studies (25), it was shown that the
overnight effect seen on glucose tolerance at breakfast after a
barley kernel evening meal corresponded to a higher concentra-
tion of plasma propionate (derived from colonic fermentation)
and a lower concentration of free fatty acids in the morning. In
addition, in a recent study (52), it was found that after different
cereal-based evening meals, the glucose response to a standard-
ized high-GI breakfast was negatively correlated to the concen-
tration of plasma propionate and positively correlated to the
concentration of fasting plasma free fatty acids. Such benefits
mediated through colonic fermentation might actually contribute
to the protective role of whole-grain diets adjunct to the devel-
opment of type 2 diabetes (3, 4), coronary artery disease (1, 5),
and the metabolic syndrome (6). However, whole-grain foods are
additionally rich in associated bioactive components such as
choline, betaine (53), minerals, plant sterols, vitamins, antioxi-
Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008
dants, and lignans (54, 55), which may add to the beneficial
effects.
In conclusion, the present study shows that certain cereal prod-
ucts with low GIs and high contents of specific indigestible
carbohydrates (RS ѿ DF) can modulate the glucose response not
only in the acute phase but also during the course of a whole day,
as well as in the perspective from a late evening meal to the
subsequent breakfast. Taken together, this information provides
additional support for metabolic benefits of foods that induce
lower acute glycemic excursions and provides a new dimension
for the design of low-GI foods with optimal contents of indigest-
ible carbohydrates for magnified metabolic benefits on blood
glucose regulation.
Mia Svensson at Applied Nutrition and Food Chemistry, Lund University,
Sweden, is gratefully acknowledged for skillful assistance with the experi-
mental work.
The contributions of the authors were as follows—ACN: coordinated the
study and was responsible for the study design, for the collection and analysis
of the data, for statistical analysis, and for writing the paper; EMÖ: was
involved in the evaluation and writing of the paper; YG: provided comments
to the results and to several practical details; IMEB: was the guarantor for the
funding of the study and was involved in the study design and writing of the
paper. None of the authors had any conflicts of interest.
REFERENCES
1. Jenkins DJ, Kendall CW, Augustin LS, et al. Glycemic index: overview
of implications in health and disease. Am J Clin Nutr 2002;76:266S–
73S.
2. Brand-Miller JC. Glycemic load and chronic disease. Nutr Rev 2003;
61:S49 –55.
3. Salmeron J, Ascherio A, Rimm EB, et al. Dietary fiber, glycemic load,
and risk of NIDDM in men. Diabetes Care 1997;20:545–50.
4. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett
WC. Dietary fiber, glycemic load, and risk of non-insulin-dependent
diabetes mellitus in women. JAMA 1997;277:472–7.
5. Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary
glycemic load, carbohydrate intake, and risk of coronary heart disease in
US women. Am J Clin Nutr 2000;71:1455– 61.
6. McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PW, Jacques PF.
Carbohydrate nutrition, insulin resistance, and the prevalence of the
metabolic syndrome in the Framingham Offspring Cohort. Diabetes
Care 2004;27:538 – 46.
7. Anderson JW, Hanna TJ, Peng X, Kryscio RJ. Whole grain foods and
heart disease risk. J Am Coll Nutr 2000;19:291S–9S.
8. McKeown NM, Meigs JB, Liu S, Wilson PW, Jacques PF. Whole-grain
intake is favorably associated with metabolic risk factors for type 2
654 NILSSON ET AL
diabetes and cardiovascular disease in the Framingham Offspring Study.
Am J Clin Nutr 2002;76:390 – 8.
9. Frost G, Leeds A, Trew G, Margara R, Dornhorst A. Insulin sensitivity
in women at risk of coronary heart disease and the effect of a low
glycemic diet. Metabolism 1998;47:1245–51.
10. Frost G, Dornhorst A. The relevance of the glycaemic index to our
understanding of dietary carbohydrates. Diabet Med 2000;17:336 – 45.
11. Rask-Madsen C, King GL. Mechanisms of disease: endothelial dysfunc-
tion in insulin resistance and diabetes. Nat Clin Pract Endocrinol Metab
2007;3:46 –56.
12. King GL, Loeken MR. Hyperglycemia-induced oxidative stress in dia-
betic complications. Histochem Cell Biol 2004;122:333– 8.
13. Ross R. Atherosclerosis—an inflammatory disease. N Engl J Med 1999;
340:115–26.
14. Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Are oxidative stress-
activated signaling pathways mediators of insulin resistance and beta-
cell dysfunction? Diabetes 2003;52:1– 8.
15. Miyazaki Y, Kawano H, Yoshida T, et al. Pancreatic B-cell function is
altered by oxidative stress induced by acute hyperglycaemia. Diabet
Med 2007;24:154 – 60.
16. Ford ES, Mokdad AH, Giles WH, Brown DW. The metabolic syndrome
and antioxidant concentrations: findings from the Third National Health
and Nutrition Examination Survey. Diabetes 2003;52:2346 –52.
17. Esposito K, Nappo F, Marfella R, et al. Inflammatory cytokine concen-
trations are acutely increased by hyperglycemia in humans: role of ox-
idative stress. Circulation 2002;106:2067–72.
18. Burdge GC, Calder PC. Plasma cytokine response during the postpran-
dial period: a potential causal process in vascular disease? Br J Nutr
2005;93:3–9.
19. Jenkins DJ, Wolever TM, Taylor RH, et al. Slow release dietary carbo-
hydrate improves second meal tolerance. Am J Clin Nutr 1982;35:1339 –
46.
20. Trinick TR, Laker MF, Johnston DG, Keir M, Buchanan KD, Alberti
KG. Effect of guar on second-meal glucose tolerance in normal man.
Clin Sci 1986;71:49 –55.
21. Liljeberg HG, Åkerberg AK, Bjorck IM. Effect of the glycemic index
and content of indigestible carbohydrates of cereal-based breakfast
meals on glucose tolerance at lunch in healthy subjects. Am J Clin Nutr
1999;69:647–55.
22. Liljeberg H, Björck I. Effects of a low-glycaemic index spaghetti meal
on glucose tolerance and lipaemia at a subsequent meal in healthy sub-
jects. Eur J Clin Nutr 2000;54:24 – 8.
23. Wolever TM, Jenkins DJ, Ocana AM, Rao VA, Collier GR. Second-
meal effect: low-glycemic-index foods eaten at dinner improve subse-
quent breakfast glycemic response. Am J Clin Nutr 1988;48:1041–7.
24. Thorburn A, Muir J, Proietto J. Carbohydrate fermentation decreases
hepatic glucose output in healthy subjects. Metabolism 1993;42:780 –5.
25. Nilsson A, Granfeldt Y, Ostman E, Preston T, Bjorck I. Effects of GI and
content of indigestible carbohydrates of cereal-based evening meals on
glucose tolerance at a subsequent standardised breakfast. Eur J Clin Nutr
2006;60:1092–9.
26. Granfeldt Y, Wu X, Bjorck I. Determination of glycaemic index; some
methodological aspects related to the analysis of carbohydrate load and
characteristics of the previous evening meal. Eur J Clin Nutr 2006;60:
104 –12.
27. Cummings JH, Pomare EW, Branch WJ, Naylor CP, Macfarlane GT.
Short chain fatty acids in human large intestine, portal, hepatic and
venous blood. Gut 1987;28:1221–7.
28. Cummings JH, Macfarlane GT, Englyst HN. Prebiotic digestion and
fermentation. Am J Clin Nutr 2001;73(suppl):415S–20S.
29. Anderson JW, Bridges SR. Short-chain fatty acid fermentation products
of plant fiber affect glucose metabolism of isolated rat hepatocytes. Proc
Soc Exp Biol Med 1984;177:372– 6.
30. Berggren AM, Nyman EM, Lundquist I, Bjorck IM. Influence of orally
and rectally administered propionate on cholesterol and glucose metab-
olism in obese rats. Br J Nutr 1996;76:287–94.
31. Liljeberg H, Bjorck I. Bioavailability of starch in bread products. Post-
prandial glucose and insulin responses in healthy subjects and in vitro
resistant starch content. Eur J Clin Nutr 1994;48:151– 63.
32. Holm J, Björck I, Drew A, Asp NG. A rapid method for the analysis of
starch. Starch/Stärke 1986;38:224 – 6.
33. Björck IME, Siljeström M. In-vivo and in-vitro digestibility of starch in
autoclaved pea and potato products. J Sci Food Agric 1992;58:541–53.
34. Åkerberg AKE, Liljeberg HGM, Granfeldt YE, Drews A, Björck IM. An
in vitro method, based on chewing, to predict resistant starch content in
foods allows parallel determination of potentially available starch and
dietary fibre. J Nutr 1998;128:651–9.
35. Asp N-G, Johansson C-G, Hallmer H, Siljeström M. Rapid enzymatic
assay of insoluble and soluble dietary fibre. J Agric Food Chem 1983;
31:476 – 82.
36. Brouns F, Björck I, Frayn KN, et al. Glycaemic index methodology. Nutr
Res Rev 2005;18:145–71.
37. Liljeberg H, Granfeldt Y, Bjorck I. Metabolic responses to starch in
bread containing intact kernels versus milled flour. Eur J Clin Nutr
1992;46:561–75.
38. Björck I, Granfeldt Y, Liljeberg H, Tovar J, Asp NG. Food properties
affecting the digestion and absorption of carbohydrates. Am J Clin Nutr
1994;59(suppl):699S–705S.
39. Granfeldt Y, Liljeberg H, Drews A, Newman R, Bjorck I. Glucose and
insulin responses to barley products: influence of food structure and
Downloaded from www.ajcn.org at Lund University Libraries on March 9, 2008
amylose-amylopectin ratio. Am J Clin Nutr 1994;59:1075– 82.
40. Granfeldt Y, Nyberg L, Bjorck I. Muesli with 4 g oat beta-glucans lowers
glucose and insulin responses after a bread meal in healthy subjects. Eur
J Clin Nutr 2007 Apr 4 [Epub ahead of print].
41. Brighenti F, Benini L, Del Rio D, et al. Colonic fermentation of indi-
gestible carbohydrates contributes to the second-meal effect. Am J Clin
Nutr 2006;83:817–22.
42. Robertson MD, Bickerton AS, Dennis AL, Vidal H, Frayn KN. Insulin-
sensitizing effects of dietary resistant starch and effects on skeletal
muscle and adipose tissue metabolism. Am J Clin Nutr 2005;82:559 – 67.
43. Robertson MD, Currie JM, Morgan LM, Jewell DP, Frayn KN. Prior
short-term consumption of resistant starch enhances postprandial insulin
sensitivity in healthy subjects. Diabetologia 2003;46:659 – 65.
44. Van Cauter E, Polonsky KS, Scheen AJ. Roles of circadian rhythmicity
and sleep in human glucose regulation. Endocr Rev 1997;18:716 –38.
45. Dos Santos ML, Aragon FF, Padovani CR, Pimenta WP. Daytime vari-
ations in glucose tolerance in people with impaired glucose tolerance.
Diabetes Res Clin Pract 2006;74:257– 62.
46. Höjlund K, Wildner-Christensen M, Eshoj O, et al. Reference intervals
for glucose, beta-cell polypeptides, and counterregulatory factors during
prolonged fasting. Am J Physiol Endocrinol Metab 2001;280:E50 – 8.
47. Delorme S, Chiasson JL. Acarbose in the prevention of cardiovascular
disease in subjects with impaired glucose tolerance and type 2 diabetes
mellitus. Curr Opin Pharmacol 2005;5:184 –9.
48. Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M.
Acarbose treatment and the risk of cardiovascular disease and hyperten-
sion in patients with impaired glucose tolerance: the STOP-NIDDM
trial. JAMA 2003;290:486 –94.
49. Båvenholm PN, Efendic S. Postprandial hyperglycaemia and vascular
damage—the benefits of acarbose. Diab Vasc Dis Res 2006;3:72–9.
50. Heliövaara MK, Teppo AM, Karonen SL, Tuominen JA, Ebeling P.
Plasma IL-6 concentration is inversely related to insulin sensitivity, and
acute-phase proteins associate with glucose and lipid metabolism in
healthy subjects. Diabetes Obes Metab 2005;7:729 –36.
51. Ceriello A. Oxidative stress and diabetes-associated complications. En-
docr Pract 2006;12(suppl):60 –2.
52. Nilsson A, Ostman E, Preston T, Bjorck I. Effects of GI vs content of
cereal fibre of the evening meal on glucose tolerance at a subsequent
standardized breakfast. Eur J Clin Nutr 2007 May 23 [Epub ahead of
print].
53. Craig SA. Betaine in human nutrition. Am J Clin Nutr 2004;80:539 – 49.
54. Anderson JW. Whole grains protect against atherosclerotic cardiovas-
cular disease. Proc Nutr Soc 2003;62:135– 42.
55. Slavin J. Why whole grains are protective: biological mechanisms. Proc
Nutr Soc 2003;62:129 –34.