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The present review examines the evidence regarding the effect of b-glucan onvariables linked to the metabolic syndrome (MetS), including appetite control,glucosecontrol,hypertension,andgutmicrobiotacomposition.Appetitecontrolcanindirectly influence MetS by inducing a decreased energy intake, and promisingresults for a b-glucan intake to decrease appetite have been found using guthormone responses and subjective appetite indicators. Beta-glucan also improvesthe glycemic index of meals and beneficially influences glucose metabolism inpatientswithtype2diabetesorMetS,aswellasinhealthysubjects.Furthermore,ablood-pressure-loweringeffectofb-glucaninhypertensivesubjectsseemsfairlywellsubstantiated. The gut microbiota composition might be an interesting target toprevent MetS, and preliminary results indicate the prebiotic potential of b-glucan.The evidence that b-glucan influences appetite control and gut microbiota in apositive way is still insufficient or difficult to interpret, and additional studies areneeded in this field. Still, much evidence indicates that increased b-glucan intakecould prevent MetS. Such evidence should encourage increased efforts toward thedevelopment of b-glucan-containing functional foods and promote the intake ofb-glucan-rich foods, with the aim of reducing healthcare costs and diseaseprevalence.
Citation preview
Role of dietary beta-glucans in the prevention ofthe metabolic syndrome
Lieselotte Cloetens, Matilda Ulmius, Anna Johansson-Persson, Björn Åkesson, and Gunilla Önning
The present review examines the evidence regarding the effect of b-glucan onvariables linked to the metabolic syndrome (MetS), including appetite control,glucose control, hypertension, and gut microbiota composition. Appetite control canindirectly influence MetS by inducing a decreased energy intake, and promisingresults for a b-glucan intake to decrease appetite have been found using guthormone responses and subjective appetite indicators. Beta-glucan also improvesthe glycemic index of meals and beneficially influences glucose metabolism inpatients with type 2 diabetes or MetS, as well as in healthy subjects. Furthermore, ablood-pressure-lowering effect of b-glucan in hypertensive subjects seems fairly wellsubstantiated. The gut microbiota composition might be an interesting target toprevent MetS, and preliminary results indicate the prebiotic potential of b-glucan.The evidence that b-glucan influences appetite control and gut microbiota in apositive way is still insufficient or difficult to interpret, and additional studies areneeded in this field. Still, much evidence indicates that increased b-glucan intakecould prevent MetS. Such evidence should encourage increased efforts toward thedevelopment of b-glucan-containing functional foods and promote the intake ofb-glucan-rich foods, with the aim of reducing healthcare costs and diseaseprevalence.© 2012 International Life Sciences Institute
INTRODUCTION
Beta-glucans are soluble fibers that are located inendosperm cell walls of cereals. They are linear polysac-charides composed of D-glucopyranosyl units linked by amixture of b-(1→3) and b-(1→4) glycosidic linkages. Oatand barley are rich sources of b-glucans, whereas othercereals like rye and wheat have a lower concentration. Thetotal amount of b-glucans in oat and barley is influencedby genetic as well as environmental conditions.1–3
Reported b-glucan content in different oat varieties cul-tivated in Sweden in 3 years varied from 3.5% to 5.7% ofthe dry matter.4 The same range has been found in barley(3.5–5.9% of the dry matter), though even higher percent-ages have been detected in some varieties.5,6 Beta-glucansin oats and barley differ with respect to their molecular
and structural properties such as molecular weight, solu-bility, ratio of b-(1→3) to b-(1→4) linkages, and confor-mation. Oat b-glucan has been reported to have a highermolecular weight than barley b-glucan.7,8 Because of theiruseful physicochemical properties, b-glucans are used inthe food industry as fat replacers, stabilizers, and thicken-ing agents. Beta-glucans have also gained much interestin the field of functional foods, since they are regarded asa potentially health-promoting food ingredient.
In 1997, the US Food and Drug Administrationapproved the use of the following health claim on food-product packages: “A diet high in soluble fiber fromwhole oats (oat bran, rolled oats and oat flour) and low insaturated fat and cholesterol may reduce the risk of heartdisease.”9 In 2005, barley (whole-grain barley and certaindry-milled barley grain products) was included as a
Affiliations: L Cloetens, M Ulmius, A Johansson-Persson, B Åkesson, and G Önning are with Biomedical Nutrition, Pure and AppliedBiochemistry, Centre for Applied Life Sciences at Lund University, Lund, Sweden.
Correspondence: L Cloetens, Biomedical Nutrition, Pure and Applied Biochemistry, PO Box 124, 221 00 Lund, Sweden. E-mail:[email protected]. Phone: +46-46-222-38-53. Fax: +46-46-222-46-11.
Key words: appetite control, dietary b-glucan, hypertension, metabolic syndrome, prebiotic
bs_bs_banner
Special Article
doi:10.1111/j.1753-4887.2012.00494.xNutrition Reviews® Vol. 70(8):444–458444
source of soluble fiber to be used in this health claim.10
Recently, the European Food Safety Authority gave a posi-tive opinion on the following health claim for foods con-taining oat b-glucan: “Regular consumption of oatb-glucans can actively lower/reduce blood LDL-cholesterol and total cholesterol.”11 A minimum dailyintake of 3 g of soluble fiber from oats and/or barley isrecommended to provide these health benefits.9,11–13 Thecholesterol-lowering properties and the reduction/prevention of cardiovascular diseases by b-glucans arewell documented. However, other health-related effects,such as control of circulating glucose and insulin levels,reduction of blood pressure, prebiotic effects, and effectson body weight loss and features of the metabolic syn-drome (MetS), have been less well described.
The International Diabetes Federation (IDF) pro-posed that MetS should be defined as a cluster of meta-bolic abnormalities that include central obesity,hypertension, low concentrations of high-density lipo-protein cholesterol, high levels of triglycerides, andhyperglycemia together with insulin resistance(Table 1).14,15 The MetS is associated with a fivefold higherrisk of type 2 diabetes and a twofold higher risk of car-diovascular diseases as compared with that of peoplewithout MetS.16 Key factors in the development of MetSinclude a diet rich in fat and saturated fatty acids, con-sumption of carbohydrates with a high glycemic index(GI), and a low dietary fiber intake. Therefore, consump-tion of a healthier diet, including, for example, cerealb-glucans, may help to prevent the MetS. The addition ofb-glucan may result in decreased appetite and, therefore,decreased energy intake, leading to weight loss anddecreased prevalence of MetS. The appetite is regulatedby gut hormones and can be evaluated by measuring the
concentration of these hormones in the blood and bysubjective appetite scores. More recently, obesity and type2 diabetes have also been associated with changes in gutmicrobial composition, such as a reduced diversity of thebacterial population.17,18 Furthermore, it has been sug-gested that such changes in the intestinal microbiota mayact as a causative factor in MetS.19,20 Gut microbiota maythus play a role in the development of insulin resistanceand low-grade inflammation; moreover, bacterialenzymes are crucial for proper degradation of food com-ponents, e.g., fiber. Changes in the gut microbiota com-position induced by consumption of probiotics and/orprebiotics could therefore indirectly help to reduce theprevalence of the MetS. Since MetS affects nearly 25% ofthe world’s adult population, it is very important to inves-tigate the contribution of dietary factors to the cause ofthis syndrome. In line with this, the IDF recommendschanges in dietary composition as a primary treatment ofMetS.14 The recommended dietary changes includereduced intake of saturated fat and total fat, increasedfiber intake, and, if appropriate, reduced salt intake.
Further development of optimal diets for patientswith MetS is needed, and the potential effects of oat andbarley b-glucans on characteristics linked to the MetS willbe reviewed in this paper. The focus will be on the effectsof b-glucans on obesity, hyperglycemia, hypertension,and a reduced diversity of gut microbiota, since the effectsof b-glucans on blood lipids have been reviewed previ-ously.12,13,21,22 A literature search has been performedusing MEDLINE®. Key words included oat b-glucan orbarley b-glucan in combination with one or more of thefollowing words: clinical trial, humans, MetS, obesity,appetite (hormones), diabetes, glucose and insulinresponse, hypertension, prebiotic, gut microbiota, and tol-
Table 1 The metabolic syndrome as defined by the International Diabetes Federation.Criterion MeasurePrimary criterion:
Central obesity Waist circumference*In European men: � 94 cmIn European women: � 80 cm
Plus any two of the following:Raised triglycerides � 1.7 mmol/L (150 mg/dL)
Or specific treatment for this lipid abnormalityReduced HDL cholesterol < 1.03 mmol/L (40 mg/dL) in males
< 1.29 mmol/L (50 mg/dL) in femalesOr specific treatment for this lipid abnormality
Raised blood pressure Systolic blood pressure � 130 mmHgOr diastolic blood pressure � 85 mmHgOr treatment of previously diagnosed hypertension
Raised plasma glucose Fasting plasma glucose � 5.6 mmol/L (100 mg/dL)Or previously diagnosed type 2 diabetes (if above 5.6 mmol/L (100 mg/dL), oral glucose
tolerance test is strongly recommended but is not necessary to confirm the presenceof the syndrome)
* If body mass index is >30 kg/m2, then central obesity can be assumed, and waist circumference does not need to be measured.Abbreviations: HDL, high-density lipoprotein.
Nutrition Reviews® Vol. 70(8):444–458 445
erance. Only articles published in English between 2000and 2010 have been included. Articles focusing on theeffect of physicochemical properties of b-glucans or thefood matrix on metabolic diseases have not beenreviewed. Intervention studies that reported only theeffects of b-glucan intake on blood lipids have beenexcluded because the cholesterol-lowering effect per se isout of the scope of the present review. In total, 33 articlesfound in the literature search were relevant to this topic,and they are summarized in Table 2. Both single-mealstudies and long-term dietary intervention studies arediscussed, and all selected studies were controlled studies.The effects of b-glucan intake on gut microbiota will alsobe discussed, but these are not listed in a table becausepublished data on humans are limited (2 articles).
CENTRAL OBESITY
A main criterion of MetS is central obesity, defined as awaist circumference �94 cm for European men and�80 cm for European women (Table 1).14 Central obesityis a more indicative parameter of the MetS than bodymass index (BMI). It can easily be measured by waistcircumference, which is related to gender and ethnicgroup. Evidence suggests that central obesity precedes thedevelopment of other abnormalities and can thus be con-sidered as a key factor in the pathogenesis of MetS.23 Thisis also emphasized by the IDF definition, making centralobesity the required component of the clinical diagnosis.Although the therapeutic efficacy of different diet pro-grams is much debated, it is clear that changes in dietaryhabits and eating patterns can prevent overweight andobesity. Regarding the epidemiological evidence, theintake of dietary fiber is inversely associated with theprevalence of overweight and obesity.24–26 Davis et al.25
reported in 2006 a lower mean daily intake of dietaryfiber by overweight and obese American subjects (9 g/day) compared with normal-weight subjects (12 g/day).These intakes are, however, far below the daily recom-mended dietary fiber intakes: 25–38 g/day in the UnitedStates, according to the Dietary Guidelines for Ameri-cans,27 at least 25 g/day in Europe, according to the Euro-pean Food Safety Authority,11 and 25–35 g/day inScandinavia, according to the Nordic Nutrition Recom-mendations.28 Furthermore, it has been demonstratedthat the consumption of whole-grain foods is associatedwith reduced long-term weight gain.29,30
Effects of beta-glucan intake onanthropometric measurements
Anthropometric measurements (e.g., body weight, BMI,waist circumference) are performed in most humandietary intervention studies. To investigate the effect of
food ingredients/products on anthropometric variablesand metabolism, it is important to design the study so thattotal energy intake and physical activity are constantduring the intervention period. Since the majority ofintervention studies performed with b-glucan do notfocus on anthropometrics, daily food intake and physicalactivity have not always been assessed. To give a generaloverview of the effects of b-glucan intake on anthropo-metric measurements, this review will examine studiesthat included patients with overweight and obesity andalso studies that included patients with features of theMetS, such as type 2 diabetes, hypercholesterolemia, orhigh blood pressure.
Most of the human dietary intervention studiesincluded in this review and that aimed to achieve anisocaloric diet did not find significant effects of b-glucan,administered at a daily dose ranging between 2.3 g and10.0 g, on body weight, BMI, or waist circumference(Table 2). For example, anthropometric variablesremained unchanged in 26 patients with elevated bloodpressure (mean baseline BMI, 32.6 � 1.0 kg/m2) duringa 12-week intervention period with 7.7 g/day oatb-glucan.31 The body weight of hypercholesterolemicsubjects also remained constant in a 6-week interventionstudy with a daily intake of 6 g of oat b-glucan.32 Liatiset al.,33 however, found a significant decrease in meanbody weight (-1.03 kg), BMI (-0.38 kg/m2), and waist cir-cumference (-1.63 cm) in 23 type 2 diabetic patients witha mean baseline BMI of 29.6 � 4.8 kg/m2 after a dailyintake of 3 g of oat b-glucan for 3 weeks compared withbaseline but not compared with the control group.
Robitaille et al. 34 studied the effect of a 4-week inter-vention diet supplemented with oat-bran-enrichedmuffins (2.31 g/day b-glucan) in overweight women. Noeffects of the b-glucan-supplemented diet were observedon body weight, BMI, or waist circumference. Bodyweight and BMI of women in the control group, however,were significantly decreased (-0.66 kg and -0.25 kg/m2,respectively) compared with values at the start of theintervention. In both groups, dietary intake did notchange during the intervention period.
In patients with high blood pressure, a minor butsignificant body weight gain (+0.7 kg) and a significantlyincreased BMI (+0.2 kg/m2, mean baseline BMI,29.6 � 0.8 kg/m2) have been observed after 12 weeks’administration of oat b-glucan.35 However, significantlyincreased body weight and BMI values were alsoobserved for the control diet. Test and control foods hada similar amount of energy and macronutrients, and dif-ferences in dietary intake over time did not differ betweenthe oat group and the wheat (control) group.
A randomized, parallel, controlled 12-week interven-tion study investigated the effectiveness of consumptionof oat b-glucan incorporated in an energy-restricted diet
Nutrition Reviews® Vol. 70(8):444–458446
Tabl
e2
Effec
tsof
b-gl
ucan
inta
keon
vari
able
slin
ked
toth
em
etab
olic
synd
rom
e.Re
fere
nce
Stud
yde
sign
Subj
ects
Dur
atio
nTy
pean
ddo
seof
b-gl
ucan
Anth
ropo
met
ry/
appe
tite
Glu
cose
and
insu
linre
spon
seBl
ood
pres
sure
Mak
ieta
l.(2
007)
31Ra
ndom
ized
,con
trol
led,
para
llel,
doub
le-b
lind
n=
60,h
yper
tens
ive
12w
eeks
Oat
b-gl
ucan
;7.7
g/da
yBo
dyw
eigh
tand
BMI:
NS
Glu
cose
:fas
ting
NS,
AUC
↓co
mpa
red
toco
ntro
lSB
P:↓
insu
bgro
up,
BMI>
31.5
kg/m
2
com
pare
dto
cont
rol
Insu
lin:f
astin
g↓
inb-
gluc
angr
oup
com
pare
dto
cont
rol,
AUC
↓co
mpa
red
toco
ntro
lD
BP:↓
insu
bgro
up,
BMI>
31.5
kg/m
2
com
pare
dto
cont
rol
Que
enan
etal
.(2
007)
32Ra
ndom
ized
,con
trol
led,
para
llel,
doub
le-b
lind
n=
75,e
leva
ted
chol
este
roll
evel
s6
wee
ksO
atb-
gluc
an;6
g/da
yBo
dyw
eigh
t:N
SG
luco
se:f
astin
gN
SN
SIn
sulin
:fas
ting
NS
Liat
iset
al.
(200
9)33
Rand
omiz
ed,c
ontr
olle
d,pa
ralle
l,do
uble
-blin
dn
=41
,typ
e2
diab
etes
3w
eeks
Oat
b-gl
ucan
brea
d;3
g/da
yBo
dyw
eigh
t,BM
I,an
dw
aist
circ
umfe
renc
e:↓
com
pare
dto
base
line
Glu
cose
:fas
ting
↓co
mpa
red
toba
selin
eIn
sulin
:fas
ting
↓co
mpa
red
toco
ntro
lH
bA1c
:↓co
mpa
red
toba
selin
e
SBP:
↓co
mpa
red
toba
selin
eIn
subg
roup
with
hype
rten
sive
patie
nts:
SBP
↓co
mpa
red
toba
selin
ean
dco
ntro
lD
BP:N
SRo
bita
ille
etal
.(2
005)
34Ra
ndom
ized
,con
trol
led,
para
llel
n=
34,o
verw
eigh
tw
omen
4w
eeks
Oat
bran
inm
uffins
;2.
31g/
day
Body
wei
ghta
ndBM
I:↓
inco
ntro
lco
mpa
red
tost
arti
nter
vent
ion
––
Dav
yet
al.
(200
2)35
Rand
omiz
ed,c
ontr
olle
d,pa
ralle
ln
=36
,hyp
erte
nsiv
em
en12
wee
ksO
atce
real
;5.5
g/da
yBo
dyw
eigh
tand
BMI:
↑co
mpa
red
toba
selin
eG
luco
se:f
astin
gN
SN
S
Wai
stci
rcum
fere
nce:
NS
Insu
lin:f
astin
gN
S
Beck
etal
.(2
010)
36Ra
ndom
ized
,con
trol
led,
para
llel,
ener
gy-
rest
ricte
d
n=
66,o
verw
eigh
tw
omen
3m
onth
sO
atb-
gluc
an;5
–6g/
day
or8–
9g/
day
Body
wei
ghta
ndw
aist
circ
umfe
renc
e:↓
inal
lgro
ups
Lept
in,G
LP,P
YY:↓
inal
lgro
ups
PYY:
↓co
mpa
red
toco
ntro
lCC
K:↑
inal
lgro
ups
Ghr
elin
:NS
Glu
cose
:fas
ting
NS
Insu
lin:f
astin
g↓
inal
lgro
ups
–
Beck
etal
.(2
009)
43Co
ntro
lled
n=
14,o
verw
eigh
tSi
ngle
adm
inis
trat
ion
Oat
b-gl
ucan
brea
kfas
tce
real
;2.2
g,3.
8g,
or5.
5g
PYY:
↑at
5.5
gco
mpa
red
toco
ntro
l,do
se-d
epen
dent
resp
onse
––
Beck
etal
.(2
009)
44Co
ntro
lled
n=
14,o
verw
eigh
tSi
ngle
adm
inis
trat
ion
Oat
b-gl
ucan
brea
kfas
tce
real
;2.2
g,3.
8g,
5.5
g,or
5.7
g
Ghr
elin
:AU
CN
SCC
K:AU
Cdo
se-r
espo
nse
effec
tfor
fem
ales
Subj
ectiv
esa
tiety
:↑
Glu
cose
:AU
CN
SIn
sulin
:AU
C↓
0–2
hat
3.8
g,5.
5g,
and
5.7
gco
mpa
red
toco
ntro
l
–
Vita
glio
neet
al.
(200
9)45
Rand
omiz
ed,c
ontr
olle
d,cr
osso
ver
n=
14,n
orm
al-w
eigh
tSi
ngle
adm
inis
trat
ion
Barle
yb-
gluc
anin
brea
d;3
gG
hrel
in:A
UC
↓PY
Y:AU
C↓
Subj
ectiv
esc
ores
fors
atie
ty↑,
fulln
ess
↑,an
dhu
nger
↓co
mpa
red
toco
ntro
l
Glu
cose
:pos
tpra
ndia
l↓co
mpa
red
toco
ntro
lIn
sulin
:pos
tpra
ndia
lNS
–
Lyly
etal
.(20
09)46
Cont
rolle
dn
=19
,BM
Iran
ge19
–28.
3kg
/m2
Sing
lead
min
istr
atio
nO
atb-
gluc
anbe
vera
ge;
5.1
gSu
bjec
tive
scor
efo
rhun
gera
ndap
petit
e:N
S(t
ende
ncy
obse
rved
)
––
Lyly
etal
.(20
10)47
Rand
omiz
ed,c
ontr
olle
dn
=29
,BM
Iran
ge18
.9–2
9.7
kg/m
2Si
ngle
adm
inis
trat
ion
Oat
b-gl
ucan
beve
rage
;2.
5g
or5
gSu
bjec
tive
scor
esfo
rsat
iety
↑an
dhu
nger
↓at
2.5
and
5g
com
pare
dto
cont
rol
––
Nutrition Reviews® Vol. 70(8):444–458 447
Tabl
e2
Co
nti
nu
edRe
fere
nce
Stud
yde
sign
Subj
ects
Dur
atio
nTy
pean
ddo
seof
b-gl
ucan
Anth
ropo
met
ry/
appe
tite
Glu
cose
and
insu
linre
spon
seBl
ood
pres
sure
Pete
rset
al.
(200
9)48
Rand
omiz
ed,c
ontr
olle
d,cr
osso
ver,
doub
le-b
lind
n=
21,B
MIr
ange
21.7
–30.
3kg
/m2
Sing
lead
min
istr
atio
nBa
rley
b-gl
ucan
brea
kfas
tand
snac
k;2
¥1.
2g
Subj
ectiv
esc
ores
fora
ppet
ite:N
S–
–
Kim
etal
.(20
06)49
Cont
rolle
dn
=19
,ove
rwei
ght
Sing
lead
min
istr
atio
nBa
rley
b-gl
ucan
cook
edce
real
;1g
or2
gSu
bjec
tive
scor
esfo
rsat
iety
:NS
Glu
cose
:AU
C↓
inw
omen
afte
r2g
inta
keco
mpa
red
toco
ntro
lor
1g
inta
ke
–
Hle
bow
icz
etal
.(2
008)
50Ra
ndom
ized
,con
trol
led,
cros
sove
r,do
uble
-blin
dn
=12
,BM
Iran
ge17
–27
kg/m
2Si
ngle
adm
inis
trat
ion
Oat
b-gl
ucan
mue
sli;
4g
Subj
ectiv
esc
ores
fors
atie
ty:N
SG
luco
se:↓
at30
min
com
pare
dto
cont
rol,
AUC
↓0–
30m
inco
mpa
red
toco
ntro
l
–
Will
iset
al.
(200
9)51
Rand
omiz
ed,c
ontr
olle
d,cr
osso
ver,
doub
le-b
lind
n=
20,B
MIr
ange
19.7
–26.
9kg
/m2
Sing
lead
min
istr
atio
nBa
rley
b-gl
ucan
+oa
tfib
erin
muffi
n;to
tal
fiber
9.4
g
Subj
ectiv
esc
ores
fors
atie
ty:N
S–
–
Jenk
ins
etal
.(2
002)
57Ra
ndom
ized
,con
trol
led,
open
-labe
l,cr
osso
ver
n=
16,t
ype
2di
abet
esSi
ngle
adm
inis
trat
ion
Oat
bran
cere
al(3
.7g)
,or
b-gl
ucan
-enr
iche
dce
real
(7.3
g)or
bar
(6.2
g)
–G
luco
se:f
astin
gN
S,AU
Can
dG
I0–
180
min
↓af
teri
ntak
eof
b-gl
ucan
cere
alan
dba
rco
mpa
red
toco
ntro
land
oat
bran
cere
al
–
Tapo
laet
al.
(200
5)58
Rand
omiz
ed,c
ontr
olle
d,re
peat
edm
easu
res
n=
12,t
ype
2di
abet
esSi
ngle
adm
inis
trat
ion
Oat
bran
flour
(9.4
g)or
oatb
ran
cris
p(3
.0g)
–G
luco
se:f
astin
gN
S,↓
at15
–45
min
and
↑at
90m
inaf
ter
oatb
ran
flour
orcr
isp
com
pare
dto
cont
rol,
AUC
0–60
min
↓af
ter
oatb
ran
flour
orcr
isp
com
pare
dto
cont
rol,
AUC
0–12
0m
in↓
afte
roat
bran
flour
com
pare
dto
cont
rol
–
Kim
etal
.(20
09)59
Rand
omiz
ed,c
ontr
olle
d,cr
osso
ver,
dose
-res
pons
e
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orm
ogly
cem
ic,
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ew
omen
with
incr
ease
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kfo
rin
sulin
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stan
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Sing
lead
min
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nBa
rley
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ucan
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at30
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r10.
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g,AU
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120
min
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–
Insu
lin:f
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ter1
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008)
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ntro
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gor
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ter4
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orm
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sulin
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ntro
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C↓
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r4g
com
pare
dto
cont
rol
Nutrition Reviews® Vol. 70(8):444–458448
Kabi
reta
l.(2
002)
62Ra
ndom
ized
,con
trol
led,
cros
sove
r,do
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etes
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Oat
b-gl
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day
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iet)
Body
wei
ght:
NS
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cose
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ting
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AUC
0–18
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GI)
com
pare
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p
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Insu
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min
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HbA
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SCu
gnet
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10)63
Rand
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Oat
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day
BMI:
NS
Glu
cose
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ting
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bA1c
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Mak
ieta
l.(2
007)
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este
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evel
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atb-
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up;
4g/
day
BMI:
NS
Glu
cose
:fas
ting
and
post
pran
dial
NS
–
Insu
lin:p
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ialN
SBi
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.(2
005)
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evel
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.(2
003)
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vate
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oles
tero
llev
els
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Barle
yb-
gluc
an;9
.9g/
day
Body
wei
ght:
NS
Glu
cose
:fas
ting
and
post
pran
dial
NS
–
Thon
dre
and
Hen
ry(2
009)
72Ra
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ized
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trol
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sove
r,si
ngle
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/m2
Sing
lead
min
istr
atio
nBa
rley
b-gl
ucan
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tbre
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rol,
AUC
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alld
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com
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gluc
ose,
AUC
↓at
4g
or8
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mpa
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tobr
ead
with
outb
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can
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GI:
↓of
brea
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ith4
gor
8g
com
pare
dto
cont
rol
Mäk
eläi
nen
etal
.(2
007)
73Ra
ndom
ized
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trol
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10,n
orm
al-w
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ngle
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ion
Oat
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or6
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cose
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Insu
lin:A
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Naz
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trat
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Oat
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ucan
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dto
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rich
pole
nta
mea
l;5
g
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netic
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ower
appe
aran
ceof
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enou
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ma
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%)c
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red
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ntro
l
–
Batt
ilana
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.(2
001)
75Co
ntro
lled
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orm
al-w
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enAd
min
istr
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nof
freq
uent
smal
lm
eals
over
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8.9
g/da
y–
Kine
tics:
slow
erap
pear
ance
ofex
ogen
ous
gluc
ose
inpl
asm
a(-
21%
)com
pare
dto
cont
rol
–
Keen
anet
al.
(200
2)78
Rand
omiz
ed,c
ontr
olle
d,pa
ralle
ln
=18
,hyp
erte
nsiv
ean
dhy
perin
sulin
emic
6w
eeks
Oat
cere
al;5
.5g/
day
Body
wei
ght:
NS
Insu
lin:f
astin
gan
dAU
C(t
ende
ncy
obse
rved
)NS
SBP:
↓co
mpa
red
toba
selin
ean
dco
ntro
lD
BP:↓
com
pare
dto
base
line
Pins
etal
.(2
002)
79Ra
ndom
ized
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trol
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para
llel
n=
88,h
yper
tens
ive
trea
ted
with
antih
yper
tens
ion
med
icat
ion
12w
eeks
Oat
cere
al;5
.4g/
day
Body
wei
ght:
NS
Glu
cose
:fas
ting
↓co
mpa
red
toco
ntro
lSB
P:↓
DBP
:NS
Abbr
evia
tions
and
sym
bols:
AUC,
area
unde
rthe
curv
e;BM
I,bo
dym
ass
inde
x;CC
K,ch
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ysto
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iast
olic
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dpr
essu
re;G
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icin
dex;
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epe
ptid
e;N
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tsig
nific
ant;
PYY,
pept
ide
YY;S
BP,s
ysto
licbl
ood
pres
sure
;↓,
sign
ifica
ntre
duct
ion;
↑,si
gnifi
cant
incr
ease
.
Nutrition Reviews® Vol. 70(8):444–458 449
in overweight women.36 The subjects consumed a mod-erate (5–6 g/day) or high (8–9 g/day) dose of b-glucan.Body weight and waist circumference were significantlydecreased within all groups, but there was no significantdifference between the groups. These findings indicatedthat the supplementation of b-glucan did not enhance theeffect of an energy-restricted diet on anthropometricvariables.
In conclusion, the effect of dietary b-glucan onanthropometric measurements remains unclear. Dose,physical properties, like molecular weight, and processingof b-glucans and food matrix may also influence theputative induced changes in anthropometric values.Moreover, the observed changes in anthropometric mea-surements largely depend on the total energy intake andphysical activity and the intake of other components. Ifbody weight loss is observed after a b-glucan interventionperiod, it is difficult to state that b-glucan is the mainfactor responsible for body weight reduction. Bodyweight reduction was actually not the primary aim inmost studies. In the literature search for this review, onlyone intervention study in which b-glucan was incorpo-rated in an energy-restricted diet was found.36 The effectsof b-glucan on appetite are discussed below.
A possible mechanism explaining the hypothesis thatdietary b-glucan could prevent central obesity is thatb-glucan increases the viscosity of the gastrointestinalchyme.37 The increased viscosity causes a delayed gastricemptying after the intake of liquid or solid meals andleads to the formation of an unstirred water layer adjacentto the mucosa that causes a slower digestion and absorp-tion of the nutrients due to reduced enzymatic activityand mucosal absorption.38,39 These physiological effectsmay signal a person to stop eating earlier than usual and,thus, decrease overall energy intake.
Effects of beta-glucan intake on appetite
One important strategy in the management of overweightand obesity is the reduction of energy intake by control ofappetite.As described earlier, b-glucans form a viscous gelmatrix that increases the viscosity of the gastrointestinalchyme after ingestion and may delay gastric emptyingand increase satiety.39–41 Gut hormones like leptin,glucagon-like peptide-1 (GLP-1), peptide YY (PYY), andcholecystokinin (CCK) suppress the appetite, whereasghrelin stimulates appetite.42 These hormones modulatefood intake on a meal-by-meal basis, and changes in guthormone concentrations may be observed after only asingle meal. Besides physiological factors, food intake isalso influenced by nonphysiological factors such ashedonic (palatability, taste, texture, odor), environmental(temperature, time of day, presence of other people),
economic (costs, availability), and social (culture, reli-gion) factors.
In a study of 14 overweight subjects, postprandialplasma levels of PYY increased after ingestion of an oatb-glucan-enriched breakfast meal compared with acontrol meal (Table 2).43 PYY is a polypeptide secretedprimarily by endocrine cells in the distal bowel and colon.It binds to the Y2 receptor in the hypothalamus. Thisreceptor inhibits the release of neuropeptide YY, a potentappetite stimulator, and thus PYY acts as suppressor offood intake. The increase in PYY area under the curve(AUC) was shown to be dose dependent within a rangefrom 2.2 g to 5.5 g of b-glucan/serving. The same researchgroup also reported a dose-response relationship betweenthe intake of b-glucan (2.2 g to 5.7 g) and postprandialplasma CCK AUC.44 However, this dose-response rela-tionship was only significant for overweight women(n = 7). CCK is secreted in the small intestine, and itssecretion is stimulated by fat- and protein-rich chyme inthe duodenum. Since stimulation of CCK inhibits gastricemptying, CCK acts as an appetite suppressor. Ghrelinlevels were not significantly changed after intake of dif-ferent doses of b-glucan.44 These observed changes in guthormones suggested that b-glucan could increase satiety.In another study confirming these results, consumptionof 100 g of bread enriched with 3 g of barley b-glucan by14 healthy subjects (mean BMI, 22.9 � 2.8 kg/m2) signifi-cantly increased the AUC of plasma PYY concentration(+16%) and significantly decreased the AUC of plasmaghrelin (-23%).45 Besides plasma PYY and ghrelin, sub-jective appetite scores were also measured in this study. Asignificantly reduced hunger sensation (-49%) and a sig-nificant increase in perceived fullness (+25%) wereobserved between 120 min and 180 min after consump-tion of the b-glucan-enriched bread compared with acontrol bread. Subjective score for satiety after intake ofb-glucan-enriched bread was only significantly differentat 120 min compared with the control bread group. Theseresults indicated an association between ghrelin and PYYresponse and appetite ratings due to intake of barleyb-glucans.
Since meal studies only show acute effects, it is alsouseful to investigate the effect of a food ingredient onappetite after a longer intervention period. A 12-weekcontrolled, energy-restricted dietary intervention in over-weight women with oat b-glucan-enriched test meals andsnacks (5–6 or 8–9 g/day b-glucan) showed a significantbody weight loss together with significantly decreasedfasting levels of leptin, GLP-1, and PYY over time.36 OnlyPYY levels were significantly different from control.Ghrelin levels did not change during the interventionperiod.
Other studies measuring subjective scores reportedby the study participants also showed an extended satiety
Nutrition Reviews® Vol. 70(8):444–458450
after consumption of a b-glucan-rich drink. The intake ofa beverage containing 5 g of oat b-glucan by 19 healthyvolunteers (mean BMI 23.2, range 19.0–28.3 kg/m2)tended to increase satiety and to decrease the desire to eatmore than intake of a beverage without fiber.46 Largeindividual variations were observed, and it was difficult todemonstrate a significant difference. Oat b-glucan addedto a beverage in a dose of 2.5 g or 5.0 g significantlyincreased the feeling of satiety and significantly decreasedhunger in 29 healthy volunteers (mean BMI 23.2, range18.9–29.7 kg/m2) compared with a control beverage.47
The effect on satiety and hunger between the differentdoses of oat b-glucan was not significantly different, indi-cating that there was no dose-response effect. The feelingof satiety was significantly lower after consumption of alow-viscosity oat b-glucan beverage compared with aftera high-viscosity oat b-glucan beverage.47 Hunger rating,however, was not affected by viscosity.
In contrast, several other studies could not confirmthat b-glucans control appetite in humans. Barleyb-glucan (2 ¥ 1.2 g) added to meal-replacement bars didnot affect satiety and appetite in 21 healthy humans(mean BMI 25.9, range 21.7–30.3 kg/m2), although theviscosity of the gastric content in vitro more than doubledwhen b-glucan derived from oat and barley was added.48
The scores for palatability did not differ between themeals. A lack of statistical significance could be due to thelow amounts of added b-glucan. However, the authorsstated that the amount of barley (8.0 g) was judged to bethe maximum amount that could feasibly be added to thebar and still retain acceptable palatability and productquality. Another study in which 1 or 2 g of barleyb-glucan was served as a hot cereal with yogurt to 19overweight subjects (mean BMI for men and women,29.2 � 0.7 kg/m2 and 31.8 � 1.2 kg/m2, respectively) didnot show significant effects regarding postprandial satietyand energy intake.49 The authors suggested that higherdoses of b-glucan are required to affect short-termsatiety. A randomized, crossover, double-blind trial with12 healthy subjects (mean BMI, 22 � 3 kg/m2) did notshow significant differences in satiety or gastric emptyingafter ingestion of yogurt with muesli containing flakesfrom oat bran (4 g of oat b-glucan) compared with yogurtwith muesli containing cornflakes.50 Another study with20 healthy volunteers (mean BMI, 24.5 � 0.7 kg/m2 and22.9 � 0.6 kg/m2 for men and women, respectively) alsofailed to show significant effects in satiety scores whenbarley b-glucan and oat fiber were added to muffins (4 gof soluble fiber added).51 On the contrary, significanteffects on satiety scores were observed when resistantstarch or corn bran was added to the muffins. This resultsuggests that added fibers will not impact satiety uni-formly and that the type of fiber must be consideredcarefully.
Six of the included 10 studies showed, using guthormone responses, that intake of b-glucan affects appe-tite and subjective indicators of appetite. More studies areneeded to document if b-glucan is effective as a weightloss treatment, as summarized in the previous section. Itis possible, however, that b-glucan intake is more effectivefor prevention of MetS than for treatment of MetS. If so,the observed changes in gut hormone concentrations andsubjective appetite ratings by b-glucan intake might helpto inhibit body weight gain.
The mechanism of action of b-glucan on appetitecontrol should be clarified to understand the discrepan-cies between the different studies. Most of the discussedpapers analyzed effects of b-glucan on appetite in healthynonobese humans, and it cannot be excluded that over-weight and obese people might show other outcomes.Moreover, it is rather difficult to directly compare theeffects observed in different studies because differentdoses, types of b-glucan (solubility, molecular weight),and food matrices, which all affect the viscosity of thechyme, have been administered to different study groups.Furthermore, the processing of fibers before adding themto a food matrix also affects the results.
HYPERGLYCEMIA
A fasting plasma glucose level higher than 5.6 mmol/L(100 mg/dL) has been defined by the IDF as a criterion ofthe MetS (Table 1). Type 2 diabetes is a chronic diseasecharacterized by high blood glucose levels resulting fromineffective use of insulin by the body (insulin resistance).A high intake of fat and a sedentary lifestyle are linked tothe development of insulin resistance and type 2 diabe-tes.52,53 A healthy diet, regular physical activity, and main-tenance of a normal body weight can prevent or delay theonset of type 2 diabetes. Moreover, previous epidemio-logical studies have demonstrated that diets with a highglycemic load and low cereal fiber content increasethe risk of developing type 2 diabetes in men andwomen.54,55
Effects of beta-glucan on blood glucose andinsulin levels
Consumption of soluble dietary fibers has been associ-ated with lower postprandial glucose and insulinresponse.56 In a randomized crossover meal study with 16type 2 diabetic patients, addition of oat b-glucan to abreakfast cereal and bar (7.3 g and 6.2 g of b-glucan,respectively), each containing 50 g of carbohydrate, sig-nificantly lowered blood glucose response and glucoseincremental AUC as compared with white bread (control)or a commercial oat bran breakfast cereal (Table 2).57 Gly-cemic response after a single administration of oat bran
Nutrition Reviews® Vol. 70(8):444–458 451
flour (9.4 g of b-glucan) to 12 type 2 diabetics was signifi-cantly decreased compared with that after 12.5 g of glu-cose.58 Moreover, the shape of the plasma glucoseresponse after ingestion of the oat bran flour was remark-ably flattened compared with that after the glucose load.On the other hand, ingestion of oat bran crisp (3.0 g ofb-glucan) had less influence on postprandial bloodglucose response. These results suggest that the amountof dietary fiber, especially b-glucan, in oat bran productsprobably explains the differences in glycemic response. Adose-response effect between barley b-glucan and glyce-mic response was observed in a study of obese womenwith increased risk for insulin resistance.59 In that study, adose range of 0–10 g was used, and the authors observedthat only the highest dose improved postprandial glyce-mic and insulin responses. In healthy nonobese subjects,significantly decreased levels of glucose and insulin wereobserved when 4 g of oat b-glucan was added to a break-fast meal, whereas supplementation with 3 g of oatb-glucan had no effect.60
After a 3-week intervention period with oat b-glucan(3 g/day) enriched bread, a significant decrease in fastingplasma glucose and a tendency to decreased fastingplasma insulin and insulin resistance index in type 2 dia-betic subjects was observed compared with baseline.33
The fasting plasma insulin and the insulin resistanceindex after oat b-glucan intervention were significantlylower than in the control group. The insulin resistanceindex quantifies insulin sensitivity and is calculated bymultiplying fasting plasma glucose (mmol/L) by fastingplasma insulin and dividing by 22.8 mmol/L.61 Otherlong-term studies did not find a significantly decreasedlevel of fasting glucose and/or insulin in type 2 diabeticpatients after giving a b-glucan-supplemented diet.62,63 Inhealthy men, consumption of a diet containing 5.7 g/dayof oat b-glucan for 2 weeks did not affect postprandialglucose or insulin response compared with a wheat(control) diet.64
The effects of b-glucan on fasting and postprandialglucose and on insulin levels have also been studied insubjects with hypertension and hypercholesterolemia.Consumption of oat cereals (5.5 g/day b-glucan) by 18men with high blood pressure did not affect fastingglucose or insulin concentrations during a 12-weekintervention period.35 In another 12-week oat b-glucan(7.7 g/day) intervention study of hypertensive subjects, asignificant decrease in fasting insulin was observed,whereas no effects on fasting glucose were observed.31 Insubjects with elevated cholesterol levels, daily consump-tion of soups supplemented with 4 g of oat b-glucan for5 weeks did not influence fasting glucose, postprandialglucose, or insulin levels compared with control.65 In aparallel study of hypercholesterolemic subjects, post-prandial glucose and insulin response were significantly
lowered after administration of a beverage containing5 g of oat b-glucan compared with control.66 On the con-trary, administration of a beverage with 5 g or 10 g ofbarley b-glucan or 10 g of oat b-glucan did not influencepostprandial glucose or insulin response. In that study,the mean molecular weight of barley b-glucan wasalmost half of that of oat b-glucan, resulting in a lowerviscosity. Since viscosity plays a major role in thedelayed absorption rate of glucose, this could explain theweaker effect of barley compared with oat. Anotherstudy in which high doses of barley b-glucan (9.9 g/day)were given for 4 weeks to men with mildly hypercholes-terolemia did not observe any effect on glucoseresponse.67
The effect of b-glucan intake on postprandial bloodglucose and insulin in hypertensive and/or hypercholes-terolemic subjects seems less pronounced compared withthat in patients with type 2 diabetes. This might beexplained by the occurrence of normal blood glucoselevels in hypertensive and/or hypercholesterolemic sub-jects. It has previously been reported that the character-istics of the subjects to be tested are important indetermining the level of reduction in blood glucoseand insulin response.68 Furthermore, blood glucoseresponse is determined mainly by gastrointestinal viscos-ity and food processing, in addition to blood glucoseelimination.68–70
Glycemic index (GI) is defined as the area underthe 2 h blood glucose response curve following theingestion of 50 g of carbohydrates from a test fooddivided by the AUC of a standard food (glucose or whitebread).71 It is known that the GI of a diet is positivelyassociated with the risk of developing type 2 diabetes.55
Low-GI diets may reduce or prevent hyperglycemia andcardiovascular risk factors in type 2 diabetes. A study of13 type 2 diabetic men showed significantly lowerplasma glucose peaks after 4 weeks of intake of a low-GIbreakfast, which contained 3 g of oat b-glucan, com-pared with a high-GI breakfast.62 In a study of patientswith type 2 diabetes, it was estimated that the GI wasreduced by 4 units per gram of oat b-glucan fiber in a50-g carbohydrate portion of food.57 The GI value ofunleavened Indian flatbread (chapatis), administered toeight healthy humans, was also significantly decreasedfrom control when 4 g or 8 g of barley b-glucan wasadded.72 However, no significant reduction in GI fromcontrol was observed after the addition of 6 g of barleyb-glucan to the flatbread. Another study with healthysubjects also reported a significantly decreased incre-mental glucose AUC after consumption of 4 g of oatb-glucan compared with 2 g of oat b-glucan.73 Afterintake of a higher dose (6 g) of oat b-glucan, no statis-tically significant differences were observed comparedwith lower doses.
Nutrition Reviews® Vol. 70(8):444–458452
A few studies have investigated the mechanisms ofaction behind the glucose- and insulin-lowering proper-ties of b-glucan. Stable isotopes have been used to evalu-ate the kinetics of glucose metabolism, and they allow themeasurement of the rate of appearance of exogenous (ameal labeled with 13C) and total glucose, along with theestimation of endogenous glucose mobilization. In a ran-domized, crossover, single-blind study of 12 healthy over-weight men (mean BMI, 27.5 � 0.3 kg/m2), the effect onglucose and insulin kinetics of adding 5 g of oat b-glucanto a polenta meal naturally rich in 13C was studied.74 It wasobserved that, over 360 min after a meal, the quantity oftotal and exogenous glucose in the plasma was similar forthe meals with and without b-glucan. However, the kinet-ics of the glycemic response differed, with less total andexogenous (-18%) glucose measured between 0 and120 min and significantly higher total and exogenousglucose measured 120–360 min after intake of theb-glucan-enriched meal. The slower appearance ofglucose in plasma after consumption of a meal supple-mented with b-glucan resulted in extended insulin excre-tion and a significantly inhibited mobilization ofendogenous glucose. Another study also observed thatexogenous glucose appearance was reduced by 21% afterthe administration of a b-glucan (8.9 g/day) supple-mented meal labeled with 13C-glucose to healthy mencompared to a meal without b-glucan.75 These studiesconfirm that it is important to evaluate the kinetics ofglucose metabolism; in addition, they show that lowerpostprandial glucose and insulin concentrations are duemainly to delayed carbohydrate absorption from the gut,which is induced by b-glucan.
This supports the theory that an increased viscosityof the chyme might play a major role in influencing post-prandial glycemia and GI. Because dietary glucoseabsorption is delayed, consumption of low-GI foods isencouraged to improve metabolic control in people withtype 2 diabetes or MetS.
Importantly, Juntunen et al. 68 found that food pro-cessing and the botanical structure of grain products havemore influence on postprandial glucose and insulinresponses than the amount of fiber or the type of cereal.Recently, the effects of molecular structure of cerealdietary fiber on mechanisms involved in blood glucoseand insulin regulation have been reviewed.76 It was con-cluded that molecular structure has a great impact onblood glucose and insulin response and that futureresearch should focus on determining the optimalmolecular structures of dietary fibers related to specificphysiological effects.
In general, most studies have demonstrated thatadministration of b-glucan could lower blood glucoseand insulin levels in patients with metabolic disorders aswell as in healthy subjects.
Effects of beta-glucan intake onglycosylated hemoglobin
An alternative parameter to diagnose and monitor diabe-tes is glycosylated hemoglobin (HbA1c). HbA1c values areproportional to the mean blood glucose concentrationover the previous 2–3 months, and therefore thisblood parameter is a measure of long-term glycemiccontrol.
A significant decrease in HbA1c levels from baselinewas observed in a randomized, parallel, double-blindstudy of type 2 diabetic subjects after a 3-week interven-tion period with oat b-glucan (3 g/day) -enriched bread(Table 2).33 The decrease in HbA1c, however, is not signifi-cantly different from that in the control group. Otherlong-term intervention studies did not report any signifi-cant difference in HbA1c when b-glucan was administeredto patients with type 2 diabetes.62,63 Further research iswarranted to evaluate the HbA1c-lowering effects ofdietary b-glucan.
HYPERTENSION
Elevated blood pressure as a component within the MetShas been defined by the IDF as a systolic blood pressureof �130 mmHg or a diastolic blood pressure of�85 mmHg (Table 1). Persistent hypertension is one ofthe main risk factors for stroke, heart attacks, and heartfailure. The first-line treatment for hypertension isweight loss achieved by dietary changes and increasedphysical activity. Even for people taking antihypertensivedrugs, lifestyle changes are strongly recommended.Results from a meta-analysis of 25 randomized, con-trolled trials have demonstrated that increased dietaryfiber intake may reduce blood pressure in patients withhypertension.77
Effects of beta-glucan intake on hypertension
A pilot trial including 18 subjects with hypertension andhyperinsulinemia showed a significant reduction of sys-tolic (-7.5 mmHg) and diastolic (-5.5 mmHg) bloodpressure after daily ingestion of 5.5 g of oat b-glucan as acereal for 6 weeks (Table 2).78 The decrease in systolicblood pressure was also significantly greater than in thecontrol group, whereas the decrease in diastolic bloodpressure was borderline significantly different from thecontrol group. In contrast, a study administering a higherdose (7.7 g/day) of oat b-glucan to hypertensive patientsfor 12 weeks found no significant changes in blood pres-sure compared with control.31 However, in a subgroup ofpatients with BMI > 31.5 kg/m2, a significant reduction insystolic (-5.6 mmHg) and diastolic (-2.1 mmHg) bloodpressure was found in the b-glucan group compared with
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the controls. Dietary changes other than soluble fiberintake could, however, explain some of the blood-pressure-lowering effect. Indeed, a tendency to reducesodium and calcium intake and increase potassium intakewas observed in patients assigned to the b-glucan group.In another study, 3-week incorporation of oat b-glucaninto bread (3 g/day) in the diet of patients with type 2diabetes also demonstrated a significant reduction of sys-tolic blood pressure (-9.1 mmHg) as compared withbaseline but not with control.33 After inclusion of only thepatients with a high blood pressure (n = 12), the effect onsystolic blood pressure was even more pronounced(-12.2 mmHg) and was significantly different both frombaseline and control. The authors suggested that thereduction of systolic blood pressure was related to weightloss. Diastolic blood pressure, however, remainedunchanged during the study. Davy et al. 35 reported nosignificant effects of oat consumption on blood pressure.In that randomized, parallel study, 36 men with elevatedblood pressure consumed oat cereals, providing 5.5 g/dayoat b-glucan, or wheat cereals for 12 weeks. A possibleexplanation for the lack of an effect by b-glucan on bloodpressure could be the observed significant increase inbody weight and BMI.
Another research group studied the influence of oatcereals on blood pressure in hypertensive patients takingantihypertension medication.79 This randomized, con-trolled, parallel study consisted of a 4-week baselinefeeding period with either oat cereals or low-fibercereals (control), followed by a 4-week medication-reduction phase and a 4-week maintenance phase. Thenumber of patients that reduced their medicationduring the intervention and maintenance phases wassignificantly higher in the oat group (73%) than in thecontrol group (42%). Moreover, patients in the oatcereal group without reduction in medication showedreduced systolic (-7 mmHg) and diastolic (-4 mmHg)blood pressure. Body weight remained unchanged inboth groups.
In conclusion, these findings indicate that increasedintake of b-glucan can reduce blood pressure and suggestthat dietary sources naturally rich in b-glucan (e.g., oatand barley) and b-glucan-supplemented foods as part of ahealthy diet could be recommended to hypertensivepatients. A decrease in blood pressure may not onlydepend on the dose of b-glucan but might also be linkedto changes in body weight, total energy, and dietaryintake, which in turn might be only partly dependent onb-glucan consumption. Mechanisms behind the blood-pressure-lowering effect of dietary fibers are, however,still unclear. More human intervention studies are neededto confirm the blood-pressure-lowering effect ofb-glucans within the MetS and to define its optimal use indifferent settings.
GUT MICROBIAL COMPOSITION
A reduced gut microbial diversity has been observed inobese people and patients with type 2 diabetes.17,18 A highdiversity of colonic microbiota is important because thebacteria have metabolic, trophic, and protective functionsthat influence the host’s health.80 Furthermore, it has beenshown that the gut microbiota is involved in the regula-tion of energy homeostasis and fat storage.81,82 Recently,gut microbiota has also been considered a possible caus-ative factor of metabolic disorders19,20 as well as a thera-peutic target through the use of probiotics and/orprebiotics.83 Beta-glucans may have a prebiotic effect inthe gut. A prebiotic is defined as a nondigestible foodingredient that beneficially affects the host by selectivelystimulating the growth and/or activity of one or a limitednumber of bacteria in the colon, thereby improving thehost’s health.84 Bifidobacteria and lactobacilli are benefi-cial colonic bacteria that can be stimulated by prebiotics.Short-chain fatty acids (SCFAs; butyric acid, propionicacid, acetic acid), which are produced by the bacteria, caninduce beneficial gastrointestinal and systemic effects.85
Although SCFA production is not a criterion to establisha prebiotic effect, it is often measured because the con-centrations of SCFA reflect the colonic fermentationprocess. Fructan-type oligosaccharides,86–88 lactulose,89
and galactooligosaccharides90 are today the best-knownprebiotics, whereas xylooligosaccharides91 and arabinoxy-lan oligosaccharides92,93 have been more recently pro-posed as potentially effective prebiotics. So far, otherplant polymers, such as b-glucan, have almost beenneglected in prebiotic research, and only a limitednumber of in vitro as well as in vivo studies have inves-tigated the prebiotic potential of b-glucans.
Prebiotic potential of beta-glucan
Jaskari et al.94 have demonstrated that oat b-glucan oligo-mers, produced by enzymatic hydrolysis of b-glucan, areused as selective substrates for Bifidobacterium and Lacto-bacillus strains in vitro. Inoculation of an anaerobic batchculture with human fecal slurries and supplementation ofan oat bran-rich preparation containing 9.43% b-glucansignificantly increased bifidobacteria and lactobacillilevels after 24 h of fermentation.95 At the same time, levelsof clostridia and anaerobes,both considered to be bacteriawith harmful properties, were decreased. In that study,fructooligosaccharide was used as a positive control of theprebiotic effect, and the effects of fructooligosaccharidewere shown to be more pronounced than those of theoat-bran-rich fraction.Another in vitro study investigatedthe anaerobic fermentation, by human fecal bacteria, ofb-glucan hydrolysates with different molecular massesderived from oat and barley.96 Levels of the Lactobacillus-
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Enterococcus group were significantly increased afterinoculation with b-glucan fractions, whereas no signifi-cant differences were observed in levels of the Bifidobac-terium genus. When b-glucan oligosaccharides, obtainedby hydrolyzation of b-glucan fractions, were added to thefermenters, levels of the Lactobacillus-Enterococcus groupand the Bifidobacterium genus were significantlyincreased. Addition of inulin to the batch culture signifi-cantly increased levels of the Lactobacillus-Enterococcusgroup as well as the Bifidobacterium genus.In both studies,the levels of SCFA were also measured.Acetic acid was themost prevalent SCFA in all cases, and the extent of itsincrease was similar between the b-glucan fractions andthe positive controls (inulin or fructooligosaccharide).Propionic acid production was higher in the case ofb-glucan fractions compared with the positive controls. Ithas been demonstrated that propionic acid inhibits fattyacid synthesis, and the elevated propionic acid levels in thepresence of b-glucan could relate to the hypocholester-olemic effect associated with b-glucan consumption.Additional in vitro data reporting the effect of b-glucanson SCFA production exist.97–99 These in-vitro-based find-ings suggest the prebiotic potential of b-glucan hydroly-sates.The effects of b-glucan are in the same range as thoseobserved with commercially available prebiotics. Forfurther evaluation,the results of in vivo animal and humanintervention trials need to be considered.
Rat experiments have demonstrated that barley-containing diets can increase the amount of cecal andcolonic Lactobacillus species, especially when high-viscosity b-glucan diets are used.100,101 Besides animalstudies, only a few human studies have studied the prebi-otic potential of b-glucan. After administration of a dietcontaining a fermented, ropy, oat-based product (3.5 g ofb-glucan/day) to 13 healthy subjects for 5 weeks, theamount of fecal total bacteria and bifidobacteria was sig-nificantly increased compared with baseline and withadministration of a fermented oat-based product (3.0 g ofb-glucan/day).102 This confirms that bifidobacteria areable to ferment b-glucan.
Recently, a randomized, placebo-controlled, double-blind human intervention trial demonstrated the prebi-otic potential of low doses of b-glucan.103 A borderlinesignificantly increased concentration of bifidobacteriawas observed after daily administration of 0.75 g of barleyb-glucan to 26 healthy subjects for 1 month. However,after grouping the subjects according to age (<50 years or�50 years), a significant bifidogenic effect was observedonly in subjects older than 50 years (n = 15). Indeed, amore pronounced effect of prebiotics in elderly popula-tions is expected, because the diversity of the microbiota,in particular the levels of bifidobacteria, is reduced byage.104,105 No clear effects on levels of lactobacilli wereobserved.
To conclude, oat and barley b-glucan has prebioticpotential and thus may help to normalize the gut micro-bial composition in patients with MetS. It is important,however, to mention that the majority of the data andpromising results are based on in vitro studies. Further-more, the possible aberrations in the composition of gutmicrobiota in people with metabolic disorders are stillunclear, and more scientific evidence is necessary to elu-cidate the relationship between gut microbial composi-tion and the MetS.
TOLERANCE TO BETA-GLUCANS
Since b-glucan is fermented by bacteria in the colon, itsconsumption can cause flatulence, bloating, andabdominal cramps, especially when its intake has sud-denly been increased. In several human interventionstudies, the influence of b-glucan on gastrointestinalsymptoms was measured. Daily intake of 0.75 g ofbarley b-glucan for 30 days by healthy subjects resultedin a significant reduction in abdominal pain and a ten-dency to an increased number of watery stools andmore days of diarrhea during the second half of theintervention as compared with placebo.103 No differ-ences between the groups were observed in flatulence orin bloating during the whole intake period. Anotherstudy, which aimed to evaluate the effects of a singleintake of barley b-glucan (1.2 g) on satiety in healthysubjects, also reported no significant effects on acutegastrointestinal symptoms.48 No gastrointestinal sideeffects were noted by overweight women after 4 weeksof intake of an oat b-glucan-enriched diet (2.31 g/day).34
Daily ingestion of 3 g of oat b-glucan by patients withtype 2 diabetes for 3 weeks did not produce any adverseeffects, including gastrointestinal symptoms.33 The con-sumption of higher doses of oat b-glucan (7.7 g/day) for12 weeks by humans with elevated blood pressure didnot increase the incidence of cramping and bloating.31
However, the incidence of diarrhea/loose stools was sig-nificantly higher in the b-glucan group than in thecontrol group. Moreover, a 28-day oral toxicity studywith a high dose of barley b-glucan (5.9 g/kg bodyweight/day) in rats suggested that b-glucan is well tol-erated, as evidenced by the absence of adverse changesin the general condition and appearance of the rats, neu-robehavioral endpoints, growth, feed and water con-sumption, ophthalmoscopy, hematology, clinicalchemistry, urinalysis, organ weights, and pathology find-ings.106 This dose was about 100-fold higher than thedose suggested by the US Food and Drug Administra-tion to lower cholesterol in humans.10
The studies reviewed here show that consumption ofa daily dose of up to 10 g of b-glucan by humans is welltolerated. Higher doses of b-glucan might not be harmful
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for human health, but doses higher than 10 g/day areusually not ingested in a single meal. Food compliance,mentioned in almost all of the long-term interventionstudies discussed here, was reported as good or very good,supporting the idea that b-glucans are well tolerated. Onestudy observed a significantly lower compliance in theb-glucan group compared with the control group31;however, the authors suggested that the lower complianceas well as the greater number of dropouts in the b-glucangroup was due to the low palatability of the b-glucan dietrather than to low tolerance.
CONCLUSION
The hypothesis that b-glucan intake prevents and/orreduces obesity is still not proven, but promising resultshave been observed for the effects of b-glucan intake ongut hormone responses and subjective indicators of appe-tite. The addition of b-glucan to a meal beneficially influ-ences glucose metabolism (including blood glucose andinsulin response) as well as the GI of the meal in patientswith type 2 diabetes or MetS and in healthy subjects. Theblood-pressure-lowering effect of b-glucan in hyperten-sive subjects seems fairly well substantiated. The gutmicrobiota might be an interesting target to preventMetS, and preliminary results indicate the prebioticpotential of b-glucan. The reduced diversity of the gutmicrobiota in subjects with MetS is a very recent findingand needs further investigation.
In general, the effects of oat b-glucan have beenstudied more intensively than those of barley b-glucan.Barley b-glucans generally have a lower viscosity, whichmay result in weaker physiological effects compared withoat b-glucans. Many factors are responsible for the out-comes in human studies, and it is rather difficult todirectly compare results from different interventionstudies and to determine the pure effect of b-glucan onvariables linked to MetS. The viscosity of gastrointestinalchyme, a key factor affecting physiological changes, isinfluenced by the source and the physicochemical prop-erties of b-glucan, the processing techniques, the foodmatrix, and the dose. Further research is warranted toevaluate whether consumption of cereals already natu-rally rich in b-glucan, such as oat and barley, has similareffects on MetS-related variables as consumption of purecereal b-glucans. Moreover, research focused on struc-tural and physicochemical features of b-glucan couldhelp to optimize the health benefits of b-glucan-enrichedfoods. Importantly, these findings could encourage theconsumption of b-glucan-rich cereals and promote addi-tional efforts toward the development of functional foodscontaining b-glucan, thereby reducing healthcare costsand disease prevalence.
Acknowledgment
Funding. The work of L. Cloetens was supported by theDruvan Research Foundation and ESPEN. The work of A.Johansson-Persson was funded by the Nordic Centre ofExcellence SYSDIET.
Declaration of interest. The authors have no relevantconflicts of interests to declare.
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