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Department of Diabetes, INSERM U341, Hôtel-Dieu Hospital, Paris and * Eridania Béghin-Say, Nutrition & Health Service, Vilvoorde Research and Development Centre, Vilvoorde, Belgium
3To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • humans • short-chain fructooligosaccharides • prebiotics • insulin • dietary fiber
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Nondigestible oligosaccharides, such as the short-chain
fructooligosaccharides (FOS), are a new category of low energy
sweeteners that share many properties with fermentable dietary fibers.
FOS are naturally occurring sugars in many plants such as onion,
asparagus, wheat, rye, triticale and Jerusalem artichokes
(Clevenger et al. 1988
). The FOS used in this study are
obtained industrially by an enzymatic action on sucrose leading to a
mixture of the following short-chain fructooligosaccharides:
kestose (glucose-fructose-fructose, GF2), nystose (GF3) and
fructosyl-nystose (GF4). The FOS are a low energy bulk ingredient
having a taste similar to that of sucrose, and physical and chemical
properties that precisely match those of sucrose in a wide range of
food applications, especially in bakery goods where they may replace
sucrose (Bornet 1994
).
The FOS, like fermentable dietary fibers, escape digestion in the small
intestine and are fermented in the cecum and the colon, producing
short-chain fatty acids (SCFA), mainly acetate, propionate and
butyrate (Hosoya et al. 1988
), which are absorbed
efficiently. Acetate can reduce plasma free fatty acids (Wolever et al. 1989
). This might be beneficial to blood glucose and
insulin sensitivity in the long term because high concentrations of
plasma free fatty acids lower tissue glucose utilization and induce
insulin resistance (Randle et al. 1963
). On the other
hand, long-term dietary supplementation with propionate has been
shown to decrease blood glucose in rats (Boillot et al. 1995
) and in humans (Todesco et al. 1991
,
Venter et al. 1990a
). Butyrate is used mainly as an
energy source by the colonocytes (Roediger and Moore 1981
).
The effects of FOS have been discussed mainly in the literature in
relation to their bifidogenic character (Bouhnik et al. 1996
and 1999
, Buddington et al. 1996
, Hidaka et al. 1986
). In addition, FOS can reduce the occurrence of colon
tumors in Min mice (Pierre et al. 1997
) and increase
calcium and magnesium absorption from the colon and rectum (Ohta et al. 1995
). There are very few studies on the effects of
long-term FOS intake on glucose and lipid metabolism in humans.
We showed recently in healthy subjects that 4 wk of 20 g/d of FOS
decreased basal hepatic glucose production but had no detectable effect
on either fasting plasma glucose and lipids or insulin-stimulated
glucose metabolism (Luo et al. 1996
). In subjects with
type 2 diabetes, consumption of FOS resulted in either unchanged
(Alles et al. 1999
) or lowered (Yamashita et al. 1984
) fasting plasma glucose and serum total cholesterol
concentrations.
Thus, this study was designed to clarify whether chronic consumption of FOS in type 2 diabetic patients would ameliorate abnormal plasma lipid and glucose concentrations and whether this amelioration might be associated with changes in hepatic glucose production and insulin resistance.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Type 2 diabetic patients (n = 12; 8 men, 4 women)
were recruited from patients attending our out-patient clinic. The
sample size was determined by fixing the probability of type I error at
0.05 and that of type II error at 0.10. The variable chosen for the
calculation of sample size was basal hepatic glucose production; the
expected difference between the two treatments was 0.30 mg/(kg · min)
and the expected SD was 0.30. A greater difference was
expected in diabetic patients than that found in normal subjects
(Luo et al. 1996
). The expected SD was
determined according to results from the literature concerning diabetic
patients. The sample size determined was more than one half the number
obtained by classical calculation for a crossover design. The clinical
and biological characteristics of these subjects are given in
Table 1
. Patients with abnormal renal, hepatic and thyroid functions as
determined by physical examination, blood cell count and standard blood
biochemical profile were excluded. Similarly, patients having had
insulin treatment even transiently were not allowed to participate in
the experiment. Ten patients were taking oral antidiabetic agents
(sulfonylurea and/or metformin) and two were receiving antidiabetic
dietary regimen alone. Five patients were being treated with
ß-blockers, ACE inhibitor and/or calcium antagonist for hypertension.
All therapies were continued throughout the study. The purpose, nature
and potential risks of the study were explained and a written informed
consent was obtained from each patient. The experimental protocol was
approved by the Ethical Committee of Hôtel-Dieu Hospital.
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Design.
The patients were randomly allocated to two periods of 4 wk of 20 g/d of either FOS or sucrose consumption with a double-blind random crossover design. We used short-chain FOS from ACTILIGHT (Béghin Meiji Industries, Neuilly sur Seine, France), which consisted of 44% 1-kestose (GF2), 46% nystose (GF3) and 10% fructosyl-nystose (GF4). We chose the short-chain FOS from ACTILIGHT because it is the most widely used FOS in France. The two treatment periods were separated by a 2-wk washout interval. The daily FOS or sucrose doses were supplied in the form of powder packed in paper bags. Patients were asked to divide their daily doses into three to four portions to sweeten coffee, tea or yogurt, for example. At the end of each treatment period, subjects were asked to return the unconsumed bags of sweetener.
Patients were asked to maintain a constant lifestyle throughout the study. Fasting blood samples were collected before and every 2 wk during the treatment period for the determination of plasma glucose, insulin, triacylglycerols and cholesterol. At the end of each treatment period, fasting blood samples were drawn to assess the concentrations of glycated hemoglobulin, fructosamine and insulin binding to erythrocytes. Patients were then subjected to an isotopic measurement of glucose turnover followed by an insulin tolerance test.
Dietary follow-up.
At the beginning of the study and every 2 wk during the treatment
periods, patients received individual counselling by a dietitian. They
were recommended to consume 45–50% of their energy intake as
carbohydrate, 13–15% as protein and 33–37% as fat. A low fiber diet
was prescribed individually according to data obtained from a dietary
questionnaires to maintain the initial energy intake and keep nutrient
proportions constant throughout the study. The low fiber diet was
prescribed to prevent intestinal side effects of the FOS. To assess
compliance wiith the dietary recommendations, patients were asked to
keep a food diary to be completed 2 d of each week including one
weekend day. Household measuring cups or spoons and food pictures were
used to quantify portion sizes of foods eaten. When records were
returned every 2 wk, the dietitian checked the contents of the records
and clarified any ambiguous information with the subject. These records
were analyzed using the computer program Profile Dossier V3 software
(Audit Conseil en Informatique Médicale, Bourges, France); its
dietary database is formed of 400 foods or groups of foods
representative of the French diet. French food contents were obtained
from Ciqual Repertory (Feinberg et al. 1991
).
Basal hepatic glucose production.
Measurements of hepatic glucose production (Darmaun et al. 1988
) were performed in the basal state at the end of each
treatment period. In the morning of the experiment at 0800 h,
after an overnight fast, one catheter was placed in an antecubital vein
for a primed and continuous (6,6-2H2) glucose
(MassTrace, Woburn, MA) infusion. Another catheter was placed in a
retrograde manner into a contralateral wrist vein for blood sampling.
Venous blood was arterialized by placing the hand in a heated box
(70°C). The priming dose of (6,6-2H2) glucose
was determined according to basal individual plasma glucose
concentrations. After the priming dose, the infusion rate of
(6,6-2H2) glucose was maintained at 3 mg/(kg
· h) for 3 h. To determine the (6,6-2H2)
glucose enrichment, blood samples were drawn at the beginning of the
isotope infusion and at 10-min intervals during the last 30 min of each
step.
The calculation of hepatic glucose production was based on the
assumption that the plasma glucose steady state was achieved
(Hother-Nielsen and Beck-Nielsen 1990
), i.e.,
Ra = i/Ep, where
i is the tracer infusion rate and Ep is
the (6,6-2H2) glucose isotopic enrichment in
the plasma.
Insulin tolerance test.
An insulin tolerance test (performed to evaluate insulin sensitivity)
measured response of blood glucose concentrations to exogenously
administered insulin. It consisted of a bolus intravenous injection of
regular insulin (Actrapid, Novo Laboratories, Boulogne-Billancourt,
France) 0.1 U/kg body weight (Akinmokun et al. 1992
). Plasma glucose was measured at 1-min intervals for 15
min from an arterialized vein. The test was performed in fasting
subjects and ended by feeding the subjects after 15 min.
The first-order rate constant for disappearance of glucose (KITT) was estimated from the slope of the regression line of the logarithm of blood glucose against time during the 3- to 15-min period after the insulin bolus.
Insulin binding to erythrocytes.
Erythrocyte insulin binding was determined by the method of
Gambhir et al. (1977)
at the end of each dietary period
in venous blood obtained from fasting subjects. The cells were
incubated with monoiodinated porcine 125I-insulin (Amersham
France SA, les Ulis, France, specific activity 74
GBq/µmol). Binding analysis was performed by means of
competitive inhibition curves and Scatchard plots. The competition
curve was considered as the curve in which the specific cell binding
fraction was plotted as a function of insulin concentration. The
maximum specific binding was the binding at tracer insulin
concentration after subtracting the nonspecific binding (binding in the
presence of 105 µg/L unlabeled insulin,
Novo Nordisk Pharmaceutique, Boulogne-Billancourt, France).
Specific insulin binding was expressed as the percentage of binding to
4.4 x 1012 cells/L.
Blood chemical assays.
Glucose was measured by the glucose oxidase method with a glucose
analyzer (Beckman, Palo Alto, CA). Insulin was determined by RIA (ERIA
Diagnostics Pasteur, Marnes la Coquette, France). The antiserum used in
the test showed a cross-reactivity of 100% with human insulin and
of 40% with proinsulin. Triglycerides (Biomérieux,
Marcy-l’Etoile, France), total cholesterol (Labintest, Aix-en
Provence, France) and HDL cholesterol (Boehringer Mannheim, Meylan,
France) were determined by enzymatic methods. Apolipoproteins A1, B and
lipoprotein (a) were determined by immunochemical assays with Behring
kits (Mauburg, Germany). Free fatty acids (Unipath, Dartilly, France)
and glycerol (Boehringer Mannheim) were determined by colorimetric
enzymatic methods. Isotopic enrichment for
(6,6-2H2) glucose was determined by capillary
gas chromatography coupled with electron-ionization mass
spectrometry (MD 800; Fisons Instruments, Manchester, UK) of a
1,2:3,5-bis (butylboronate)-6-acetyl-
-D-glucofuranose.
Ions of nominal mass 297 and 299, representing natural and enriched
(two deuterium atom) fragments, respectively, were detected and the
percentage enrichment was calculated.
Statistical methods.
The validity of the crossover design was tested by an analysis of covariance of baseline results of the second period with baseline results of the first period as the covariable and the treatment of the first period as the main factor. If an effect of treatment were detected, the crossover design should be rejected; in that case, only the results of the first period could be used for statistical analysis.
If the crossover design was validated, the effects of FOS and sucrose were compared by a multiple ANOVA followed by a post-hoc test (Least Significant Difference test). The main factors considered in the analysis were the following: treatment (with two levels, i.e., FOS and sucrose); time (with three levels, i.e., baseline, 2 wk and 4 wk); and order of randomization (with two levels). Variables not normally distributed, such as plasma glucose, insulin and lipids, were subjected to logarithmic transformation before statistical comparisons.
All statistical analyses were performed using CSS statistical package (StatSoft, Tulsa, OK). Results were considered significant when P < 0.05. Data are expressed as x ± SEM
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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According to self-report, subjects’ lifestyles remained constant throughout the study. Patients adhered to the FOS and the sucrose regimens without any difficulty. Nobody complained of any adverse symptoms during the dietary periods. The treatment of diabetes was maintained throughout the study for each of the patients. Daily intakes of total energy, carbohydrates, proteins, saturated, monounsaturated and polyunsaturated fatty acids and cholesterol were unchanged. As recommended, fiber intake was low and comparable during the two periods. The body weights of the subjects remained stable during the study.
Plasma variables.
Plasma glucose and insulin, serum triglyceride, total and HDL
cholesterol, calculated LDL cholesterol, apolipoproteins A1, B and
lipoprotein (a) concentrations remained constant throughout the study
in fasting subjects and did not differ in the sucrose and FOS periods
(Table 2
). Hemoglobin A1c, fructosamine and serum glycerol and free fatty acid
concentrations, which were measured at the end of each period, were not
different between the two treatments.
|
In comparison with sucrose ingestion, 4 wk of FOS supplementation did
not affect the maximum specific insulin binding (B/F) to erythrocytes
(Table 2)
.
Insulin tolerance test.
After intravenous injection of insulin, blood glucose concentration
began to fall after 3 min (Fig. 1
). The regression lines of the mean logarithm of blood glucose against
time were superimposed for the two periods (Fig. 1)
. The mean glucose
disappearance rate, KITT, was 0.011
± 0.001 mmol/L after 4 wk of FOS treatment and 0.010 ± 0.001 mmol/L after the sucrose period (Table 2)
. There was no
significant difference in the glucose disappearance rate between the
two periods.
|
Basal hepatic glucose production did not differ after the FOS and
sucrose periods (Table 2)
.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, Gelding et al. 1994
). In this study, the mean glucose disappearance rate was
only half of the values found in the study of Akinmokun et al. (1992)
(KITT = 0.010 ± 0.001 vs. 0.020 ± 0.01), suggesting a more severe insulin
resistance. This was consistent with the fasting plasma glucose values,
which were much higher in the patients of this study (9.71 ± 0.53
mmol/L) than in those in the study of Akinmokun et al. (6.8 ± 1.8
mmol/L). This insulin resistance, however, was not ameliorated by
chronic consumption of FOS. In rats, 10% FOS in the diet for 3 wk
prevented insulin resistance in sucrose-fed rats (Rizkalla,
Berni-Canani, Kabir and Slama, unpublished results). In a study on
baboons, Venter et al. (1990b)
showed that consumption
of 5.7 g/d of propionic acid, one of the fermentation products of FOS,
resulted in a lower glycemic response to an oral glucose tolerance
test, suggesting ameliorated insulin sensitivity. However, in healthy
subjects, an acute ileal perfusion of 0.3 mmol SCFA/min (60% acetate,
25% propionate, 15% butyrate) for 18 h had no effect on basal
hepatic glucose production and insulin sensitivity measured by
three-step euglycemic-hyperinsulinic clamp (Alamowitch et al. 1996
). Indeed, in the above-mentioned studies, human
subjects received lower doses of FOS and SCFA per unit body weight than
did animals. In addition, although results from the literature show
that the FOS are fermented in the cecum and the colon, producing SCFA
(Hosoya et al. 1988
), we did not measure the production
of the SCFA in colon or in blood in this study. Therefore, we should
not relate our results only to SCFA.
In the literature, studies investigating the effects of chronic
consumption of FOS by type 2 diabetics on plasma glucose and lipid
concentrations gave divergent results (Alles et al. 1999
, Yamashita et al. 1984
). Yamashita et al. (1984)
showed that consumption of 8 g FOS/d for
14 d resulted in a reduced fasting glycemia in type 2 diabetic
patients. However, no details concerning results of dietary regimens
were given. It is therefore difficult to conclude whether the decrease
in fasting glycemia was due to FOS intake or to changes in dietary
regimen. In this study, daily energy and macronutrient intake, as well
as body weight, remained stable during the 4-wk FOS and sucrose
periods. Thus, we can deduce that the stable glycemia during the FOS
and sucrose treatments was not affected by diet or body weight changes.
The results of Alles et al. (1999)
are consistent with
our results, i.e, consumption of 15 g FOS/d for 20 d by type
2 diabetic patients had no major effect on blood glucose and lipids. In
normal rats, a diet rich in FOS did result in a decrease in plasma
glucose (Agheli et al. 1998
). The different results
obtained in rats and humans may be explained by species differences,
pathologic state (normal or diabetic) and by the relatively different
doses used in animals and humans. Chronic high dietary intake of
propionate, one of the fermentation products of FOS, has been shown to
lower plasma glucose in rats (Boillot et al. 1995
) and
healthy humans (Todesco et al. 1991
, Venter et al. 1990a
). Acute administration of propionate, however, has
produced varying results, particularly for glycemia. After healthy
subjects consumed propionate-enriched bread, the area under the
blood glucose curve was reduced by 47.6% compared with subjects
consuming nonenriched white bread (Todesco et al. 1991
).
Rectal infusion of propionate raised serum glucose in healthy subjects
(Wolever et al. 1991
). Another acute study in healthy
men (Laurent et al. 1995
) showed that a 3-h gastric
infusion of acetate, propionate or acetate plus propionate had no
effect on either fasting glycemia or basal hepatic glucose production.
It is therefore necessary to take into account the route of
administration and duration of treatment to explain effects of dietary
manipulations on glucose metabolism and insulin sensitivity.
In a previous study in healthy subjects, we showed that 4 wk of 20 g/d
of FOS decreased basal hepatic glucose production (Luo et al. 1996
). In the type 2 diabetics studied here, however, the same
dose of FOS for the same duration had no effect on basal hepatic
glucose production. The subjects had had type 2 diabetes for ~11 y.
Their glucose metabolism might not be modified so easily by 20 g
FOS/d as that of healthy subjects, who had only a small reduction in
basal hepatic glucose production (6%) after the FOS treatment.
The chronic consumption of 20 g FOS for 4 wk did not modify plasma
lipids [triglycerides, total and HDL cholesterol, free fatty acids,
glycerol, apolipoproteins A1, B and lipoprotein (a)]. However, a diet
rich in FOS can lower blood triacylglycerols and/or cholesterol in
normal (Fiordaliso et al. 1995
, Kok et al. 1996
), insulin-resistant (Agheli et al. 1998
) and high fat–fed (Kok et al. 1998
) rats.
The decrease in blood triacylglycerol concentrations was due to lowered
hepatic fatty acid synthase activity (Agheli et al. 1998
, Kok et al. 1996
) and consequently,
decreased hepatocyte triacylglycerol production (Fiordaliso et al. 1995
, Kok et al. 1996
). These modifications
in liver metabolism may be mediated by the short-chain fatty acids
produced during the colonic fermentation of FOS. Acute infusion of SCFA
to healthy subjects, by either the rectal (Wolever et al. 1991
) or gastric (Laurent et al. 1995
) route,
decreased serum free fatty acid concentrations. Rectal infusion of
acetate alone may raise serum cholesterol, but the addition of
propionate to acetate resulted in no significant rise in cholesterol
(Wolever et al. 1991
). Chronic ingestion of 7.5 g
sodium propionate daily for 7 wk by healthy women increased serum HDL
cholesterol (Venter et al. 1990a
), a protective factor
against cardiovascular diseases.
The absence of any effect of FOS in this study might be related to the
relatively small doses used in the subjects. Previous studies showed
that a dose of 20 g/d in normal subjects was digested slightly in the
small intestine; however, the portion reaching the colon (89%) was
fermented completely by colonic flora (Molis et al. 1996
). Another study on gastrointestinal tolerance showed that
slight symptoms of intolerance to FOS such as excessive flatus occurred
when subjects ingested >30 g FOS/d (Briet et al. 1995
).
Subjects in this study did not complain of any secondary effects of the
FOS at the 20 g/d dose. Therefore, we considered 20 g/d to be a
reasonable dose in diabetic patients. Indeed, Yamashita et al. (1984)
found that 8 g FOS/d for 2 wk in NIDDM patient
lowered fasting serum cholesterol but not triacylglycerol
concentrations. The apparent discrepancies between this study and that
of Yamashita et al. may be related to the differing blood lipid status
of patients and the stability of the dietary regimen during the
studies.
In conclusion, 4 wk of daily ingestion of 20 g of short-chain fructooligosaccharides had no effect on glucose and lipid metabolism in type 2 diabetic subjects. Further studies are required to clarify whether longer term and/or higher doses of FOS might affect glucose and lipid control of type 2 diabetic patients that are less severely affected.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Current address: Department of Diabetes, UCL DIAB 5474, Av. Hippocrate, Bruxelles, Belgium.
Manuscript received October 6, 1999. Initial review completed November 23, 1999. Revision accepted January 9, 2000.
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