Review

The physiological and rheological effects of foods supplemented with guar gum
K.T. Roberts
Guelph Food Research Centre, Agriculture and Agri-Food Canada, 93 Stone Road West, Guelph, ON, Canada N1G 5C9
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, ON, Canada N1G 2W1
a b s t r a c t a r t i c l e i n f o
Article history:
Received 8 November 2010
Accepted 16 January 2011
Keywords:
Guar gum
Glycemia
The high molecular weight polysaccharide Guar gum has a plethora of uses in the food, pharmaceutical and
paint industries. This polysaccharide is also employed as a dietary bre, but the quantity used in food is
limited due to its viscous properties. Guar gum may be modied enzymatically or chemically to reduce its
molecular weight and by extension its viscosity. This modication though is believed to reduce its
physiological efcacy, for example the attenuation of postprandial glycemia. However, a number of studies
have shown the viscosity effects alone of this bre in vitro and in vivo is not always correlated with blunted
glycemia. The absolute mechanisms behind the benets seen with guar gum consumption are not known and
studies have shown factors such as food composition, food matrix and food and bre processing conditions
may all play a signicant role.
2011 Elsevier Ltd. All rights reserved.
Contents
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1109
2. In vitro and rheological effects of guar gum supplementation to foods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1110
3. Rheological and physiological effects of guar gum consumption in animal studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1111
4. Rheological and physiological effects of guar gum consumption in human studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1112
5. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1113
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1113
1. Introduction
Guar bean (Cyamopis tetragonoloba) is an annual legume cultivated
principally in India and Pakistan and to a lesser extent in the United
States. Guar gumis a coldwater soluble polysaccharide derivedfromthe
endosperm of guar beans by extraction. This polysaccharide consists of
galactomannan at a ratio of 2:1 mannose to galactose (M/G) (Kulicke,
Eidam, Kath, Kix, & Kull, 1996). Generally, galactomannans are
composed of a mannose backbone or main chain, with galactose
residues or side chains. Therefore with respect to guar gum, for every
two mannose units there is one galactose side chain. There are a number
of galactomannans employed industrially, namely tara gumwith a M/G
ratio of 3:1, locust bean gum with a M/G ratio of 4:1 (Butt, Shahzadi,
Sharif, &Nasir, 2007; Kulicke et al., 1996) andfenugreekgumwitha M/G
ratio of 1:1. Based on these ratios guar gumis most similar to fenugreek
gum than the other aforementioned galactomannans.
Guar gum is mainly composed of high molecular weight poly-
saccharides with a molecular weight range of 50,000 to 8,000,000 Da
(Kawamura, 2008). Guar gum has a plethora of uses, mainly as an
additive in the food industry. Typically guar gum is incorporated into
foods at 1 g/100 g to facilitate gelling, thickening, rming and
emulsication of food products (Flammang, Kendall, Baumgartner,
Slagle, &Choe, 2006). Its high viscosity is a limiting factor for addition to
food products at levels above 1% and consequently guar gum may be
processed into Partially Hydrolysed Guar Gum (PHGG), in order to
reduce its viscosity. Guar gum may also be used as a source of soluble
dietary bre in food products and has been assessed to be safe at usage
levels of 20 g per day (Flammang et al., 2006; Grabitske & Slavin, 2009;
Kawamura, 2008; Slavin & Greenberg, 2003).
The high viscosity of guar gumdietary bre, which sometimes poses
a problemwith food application at physiologically relevant amounts, is
ironically believed to be the reason for its reduction of postprandial
glycemia (Flammang et al., 2006; Yamada et al., 1999). Unfortunately,
Food Research International 44 (2011) 11091114
Department of Human Health and Nutritional Sciences, University of Guelph,
Guelph, ON, Canada N1G 2W1. Tel.: +1 519 780 8028; fax: +1 519 829 2600.
E-mail address: krober04@uoguelph.ca.
0963-9969/$ see front matter 2011 Elsevier Ltd. All rights reserved.
doi:10.1016/j.foodres.2011.01.065
Contents lists available at ScienceDirect
Food Research International
j our nal homepage: www. el sevi er. com/ l ocat e/ f oodr es
foods with physiologically relevant quantities of viscous bres have
very low consumer acceptability. These foods have a slimy mouth feel
and also cause tooth packing. These poor qualities can be alleviated
by reducing the average molecular weight of galactomannans like
guar gum. The drawback though is that reduction in molecular weight
has been associated with the loss of clinical efcacy (Williams et al.,
2004). According to Butt et al. (2007) a number of clinical studies (both
long term and short term) have shown a reduction in postprandial
glycemia and insulinemia on consumption of guar gum, with the
mechanismbeing attributed to an increased transit time in the stomach
and small intestine, which may have been due to the viscosity of the
meal hindering the access of glucose to the epithelium.
Due to the varietyof uses of guar guminits native or PHGGforms the
supply of this product cannot keep up with demand and guar gum is
considered the most signicant galactomannan employed industrially
(Butt et al., 2007; Kulicke et al., 1996). The modication of guar gumto
reduce its viscositymay affect the benecial physiological effects usually
associated with soluble bre consumption. PHGG (modied through
enzymatic processing) was found to have the same chemical structure
as the original guar gum, but with a signicantly reduced molecular
weight of around 20,000 Da and one-tenth the original chain length.
These modications reduced the viscosity of a solution containing 5%
PHGG to below 10 m Pa s, while a solution of 1% guar gum had a
viscosity of 2000to3000 m Pa s (Yoon, Chu, &Juneja, 2008). Fortunately
though this PHGG was manufactured by enzymatic hydrolysis and the
processing conditions did not cause extensive polymerization of the
gum. Some processing conditions such as high temperatures and wet
heat treatment have been found to alter physiochemical properties of
dietary bre (Nyman, 2003).
According to Nyman (2003) a lowering of the molecular weight of
bre may result in changes in metabolic effects, through reduced
viscosity and bre hydration capacity. The physiological effects of guar
gumare mostly but not exclusively determined by its ability to increase
digesta viscosityinthe stomachandsmall intestine (Wang, Ellis, &Ross-
Murphy, 2003). The enzymatically derived PHGG commercially known
as Sunbre gave the same physiological results as the original guar gum.
It was proposed that the enzymatic processing mirrored digestion and
so this product should simply be thought of as pre-digested guar gum
(Yoon et al., 2008).
Not all guar gum derivatives are produced the same, as some
commercially available guar gum derivatives are produced through
chemical modication, for example the reaction of guar galactomannan
with propylene oxide (Zhang, Kong, & Hui, 2007; Zhang, Zhou, & Hui
2005). This chemical modication of guar gum facilitates a broadened
application of its derivatives in the food, paint and pigment, personal care
and pharmaceutical industries to name a few. The drawback though is
when Zhang et al. (2005, 2007) conducted their physicochemical studies
on the guar gum derivatives, carboxymethyl-o-hydroxypropyl guar gum
(CMHPG), O-2-hydroxy-3-trimethylammonio propyl guar gum (HTPG)
and O-carboxymethyl-o-2-hydroxy-3-trimethylammonio propyl guar
(CMHTPG) no reference was made of the physiological effects.
Therefore, these commercially available, chemically derived products
may not be comparable with the enzymatically derived PHGG, which
may cause confusion in the literature if these products are applied to
food for physiological studies, as there may be varied physiological
results.
Furthermore, according to Cui and Roberts (2009) and Adam and
Westerterp-Plantenga (2005) there has been mixed results for bre
supplemented food, for example the application of -glucan to bread.
These inconsistent results have been attributed to differences in
processing conditions of the food and the bre, variations in plant
genetics, varied environments during harvesting and the degree of
purity of the bre. Purity differences are extremely signicant as the
physicochemical characteristics like viscosity and molecular weight
may be compromised, which may ultimately impact the physiological
effects of food supplemented with dietary bre.
The variationinresults seenfor the physiological effects of functional
foods and nutraceuticals in the literature has serious implications for
health claims. Health claims on products are now growing in
importance for manufacturers because of positive consumer perception
attributed to these products and a corresponding rapid increase in sales
andmarket share for these products. AccordingtoL'Abbe, Dumais, Chao,
and Junkins (2008) manufacturers are driven to have health claims for
their foodproducts due toa strong market fuelledbyconsumers andthe
media, due to the scientic link between diet, health and disease. Health
claims give manufacturers a competitive advantage and Jew, Vanstone,
Antoine, and Jones (2008) proposed that the potential for increased
sales due to health claims may translate to a 20% increase in sales.
Functional foods andnutraceuticals are more expensive andhavehigher
prot margins thancorrespondingconventional products. Anadditional
incentive for companies to enter this market is that the estimated
demand for these products in Canada is estimated at CAD$ 12 billion
(Scott Wolfe Management Inc., 2002).
The objective of this paper is to look at the glycemic and rheological
effects of foods supplementedwithguar gumsoluble dietary bre, when
this galactomannan is employed as a functional food or nutraceutical.
2. In vitro and rheological effects of guar gum supplementation
to foods
There has been an alarming growth in non-communicable diseases
such as cardiovascular disease, diabetes and cancer, which has been
linkedtotheover consumptionof highfat, highcaloriefoods (Brennan&
Tudorica, 2008). The over consumption of food carbohydrate and sugars
has alsobeena source of concernand a joint FAO/WHOreport has called
for a decrease in the consumption of sugars, fat and alcohol and a
corresponding increase in total dietary bre consumption (Brennan &
Tudorica, 2008).
Attention has beenfocused onthe carbohydrate content of food, due
to the postprandial glycemic effect of carbohydrate consumption. The
increase in postprandial glycemia seen with the ingestion of high
carbohydrate and high starch foods has been shown to be tempered by
non-starch polysaccharides like guar gum, through the alteration of
starchhydrolysis. The mechanisms for the reductioninstarchhydrolysis
and ultimately reduced postprandial glycemia are not fully understood
(Brennan, Blake, Ellis, & Schoeld, 1996; Brennan, Monro, & Brennan,
2008; Brennan, Suter, Luethi, Matia-Merino, & Qvortrup, 2008).
For starch to be hydrolysed for glucose liberation, the starch must be
converted from its native form to the gelatinised form. Gelatinisation is
the process whereby starch granules swell in the presence of moisture
and heat. Gelatinisationcauses melting of the starchcrystalline network
by disrupting hydrogen bonds, resulting in an amorphous material
which is susceptible to enzymatic hydrolysis. Some foods, like Scottish
shortbread, have a low moisture content, resulting in limited starch
gelatinisation on cooking, as the starch remains in its native form and
therefore cannot be digested(Funami et al., 2005; Tester &Sommerville,
2003).
Guar gum is believed to compete with starch for water in food
systems and prevent starch gelatinisation, by preventing starch from
accessing water (Tester & Sommerville, 2003). Additional theories have
been proposed for reduced starch hydrolysis in the presence of
non-starch polysaccharides like guar gum. One theory is guar gum
reduces hydrolysis and hence digestionrate by forming a barrier around
starch granules, rendering starch resistant to enzymatic degradation
(Brennan et al., 1996; Tester & Sommerville, 2003).
Therefore, when evaluating the postprandial effects of carbohydrate
foods containing NSP like guar gum the viscosity and hydrolysis effects
(using in vitro starch digestion) may be equally important, to gauge the
possible benets in vivo. Brennan, Suter, Luethi, Matia-Merino and
Qvortrup (2008) looked at the effects of guar gum, locust bean gumand
arabic gum on wheat starch and wheat our viscosity and their effects
on in vitro starch hydrolysis. They found that both guar gum and locust
1110 K.T. Roberts / Food Research International 44 (2011) 11091114
bean gum elevated the peak and nal viscosities of the starch and our
pastes, while arabic gum signicantly reduced the viscosities of the
pastes. Furthermore, guar gum and locust bean gum reduced starch
hydrolysis of gels containing wheat our or wheat starch, while gum
arabic actually enhanced starch degradation. These results if applied
from an in vivo perspective may indicate the ability of gum arabic to
actually increase postprandial glycemia. Brennan, Suter et al. (2008)
concluded that the extent of starch hydrolysis was dependant on
viscosity changes seen with the NSP, in this experiment.
Tester and Sommerville (2003) also found a restriction of starch
hydrolysis with NSP addition to wheat, normal maize starch and waxy
maize starch. This reduction in hydrolysis was related to a reduction in
water accessibility by starch, but the authors also found that NSPs
reduced the amount of amylose leached fromwheat and normal maize
starch, while increasing the leachate in waxy maize starch. These
authors further highlighted the fact that different starch sources exhibit
varying gelatinisation and swelling properties, which may be another
factor causing differences in published studies evaluating glycemic
results.
Sudhakar, Singhal, and Kulkarni (1996) looked at the rheological
effects of guar gum and locust bean gum on corn starch and waxy
amaranth starch. They found that peak viscosity and cold paste
viscosity was higher when guar gumwas mixed with amaranth starch
than corn starch. Additionally, there seemed to be a stronger
synergism between guar gum and starch than locust bean gum and
starch. Shi and BeMiller (2001) found that specic starch-gum
pairings caused viscosity increases, for example normal corn starch
with guar gum, normal corn starch with xanthan gum and waxy rice
starch with guar gum. The viscosity increasing effects were attributed
to amylosegum interactions. Some starch gum pairings resulted in
no signicant increase in viscosity, for example guar gum and tapioca
(cassava) starch. These authors also suggested that amylose from
potato and tapioca interacted differently than amylose from cereals.
It may also be possible that starch from durumwheat and starch from
common or bread wheat may also interact differently with hydrocol-
loids in food systems.
Brennan and Tudorica (2008) used durum wheat to produce pasta
supplemented with dietary bre (inulin, guar gum, pea bre, locust
bean gum, xanthan gum, bamboo bre and -glucan enriched our)
and determined starch digestibility in vitro. They conrmed that all
pasta with bre became fully gelatinised. They found that soluble
dietary bre, for example guar gum, reduced the starch digestion rate,
although samples with 2.5%, 5% and 7.5% dietary bre were not
signicant from each other at 150 or 180 min. However, samples
containing 7.5% and 10% dietary bre had a signicantly reduced
quantity of starch being digested after 300 min, when compared to
samples containing 2.5% and 5% dietary bre. Additionally, 10%
dietary bre supplemented pasta gave a signicantly lower starch
hydrolysis when compared with the other treatments, a pasta control
and a bread reference.
Scanning electron microscopy (SEM) data by Brennan and Tudorica
(2008) indicated that the integrity of the starch was seemingly
preserved by a continuous protein network for the control pasta, while
for pastas containingsolubledietary bre, inadditiontothewheat starch
granules beingsurroundedby a proteinmatrix, the starchitself appeared
to be encapsulated with a mucilaginous like layer. Brennan et al. (1996)
also found this halo effect, where guar gum seemed to coat starch
granules in a bread sample, before and after in vivo digestion in pigs.
In another study Brennan, Monro et al. (2008) evaluated the effects
of the addition of dietary bre (wheat bran, guar gum, inulin, hi-maize
and swede) at 5%, 10% and 15% on a breakfast cereal before and after
extrusion. They found the viscosity of the rawproduct to be higher than
that of the extruded product, with guar gum exhibiting the highest
incremental peak and nal viscosities between the bres. In vitro starch
digestion of the breakfast cereals alongside a control showed bre
decreased readily digestible starch, while the quantity of slowly
digestible starch had increased, which may result in blunted postpran-
dial glycemia in vivo.
Reduced starchhydrolysis could therefore be attributed to a number
of factors including, but not limitedto; (1) Reducedstarchgelatinization
(2) Inhibition of starch swelling despite being gelatinized (3) An
interference with amylose leaching (Tester & Sommerville, 2003) (4)
The halo effect where guar gum coats the starch granule causing
inhibition of enzyme activity and (Brennan et al., 1996) (5) An increase
in viscosity which may limit enzyme accessibility to starch (Brennan,
Suter et al., 2008). The physical association between starch and guar
gum (halo effect) may explain the lack of difference in physiological
results between PHGG, derived through enzymatic processing, which
has a low viscosity and high molecular weight guar gum with a high
viscosity, as well as the reducedglucose absorptionseeninpigs, without
a meaningful increase in viscosity in the work by Brennan et al. (1996).
3. Rheological andphysiological effects of guar gumconsumptionin
animal studies
Owusu-Asiedu et al. (2006) alsolookedat the effects of guar gumon
digesta passage in grower pigs compared to cellulose and a control. This
experiment showed that guar gum reduced digesta passage rate in the
small intestine by 26%, while cellulose reduced digesta passage rate by
18%. Unlikethe previous study byBrennanet al. (1996) where there was
no viscosity increase in digesta, guar gumincreased the viscosity of ileal
digesta by 72% in this study, while the increase seen for cellulose was
76%. The control diet, guar gumdiet and cellulose diet gave viscosities of
1.52 cP, 5.57 cPand6.35 cPrespectively. Only guar gumloweredplasma
glucose after feeding (60 min) by 8.4 mg/dL. Additionally, guar gum
increased digesta retention time in the ileum, but there was no increase
in digesta retention with cellulose. The viscosity alone was apparently
not predictive of postprandial glycemia, as cellulose gave a higher
viscosity than guar gum but did not cause glucose blunting.
Cameron-Smith, Collier, and O'Dea (1994) also found that the
viscosity of digesta in the gastrointestinal tract (GI) of rats was not
indicative of postprandial glycemia. These authors evaluatedthe apparent
viscosity of digesta in the GI tract of rats containing the soluble dietary
bres guar gum, xanthan gum and methylcellulose and the insoluble
dietary bre wheat bran and attempted to correlate viscosity with
glycemic response. Wheat brandidgivethehighest postprandial glycemic
response, as the incremental area under the glucose curve, at 338 mmol/
L/min. Although xanthan, guar and methylcellulose gave approximate
viscosities of 5000 cP, 100 cP and 83 cP respectively, there was no
signicant difference inthe area under the glucose curve, whichwere 237,
290 and 316 mmol/L/min for xanthan, guar gum and methylcellulose
respectively. Therefore, these results did not mirror the signicant
difference seen in viscosity between xanthan and the other two soluble
dietary bres.
Consequently, it is impractical to compare studies evaluating viscosity,
even digesta viscosity as most authors do not characterise the bre used.
Both Owusu-Asiedu et al. (2006) and Cameron-Smith et al. (1994)
evaluated the inuence of viscosity on postprandial glycemia, but neither
study gave a chemical evaluation of the dietary bre used for example
informationonmolecular weight andthepurity of the bres. Additionally,
according to Cameron-Smith et al. (1994), variations inthe preparationof
bres, the different concentrations in the diets and the diversity in
measurement procedures all hinder direct comparison of data between
studies. Hence, contradictory results seem inevitable when evaluating
bre's role in postprandial glycemia.
Fortunately, many researchers have attempted to understand the
mechanisms behind the attenuation of postprandial glycemia on
consumption of soluble dietary bre. Poksay and Schneeman (1983)
found that when a 10% guar gum diet was fed to rats there was a
signicant reduction in feed consumption when compared with a bre
free diet and a stock diet, despite the guar gum diet having a lower
caloric density. Rats fed with the guar gum had a more distended
1111 K.T. Roberts / Food Research International 44 (2011) 11091114
intestine, as a larger quantity of food remained in the gut, which seems
tobea paradoxas rats fedwiththe other twodiets consumedmore food.
Furthermore, Poksay and Schneeman (1983) proposed that the heavier
intestinal weight seen for rats consuming guar gum may be due to an
increase in intestinal tissue mass. It has been proposed that the
consumption of gel forming bres may change the morphology of the
intestine, to better handle the bulk as well as the reduced rate of
digestion and absorption.
Cameron-Smith, Habito, Barnett, and Collier (1997) expandedtheir
search for the mechanisms behind bre's glycemia attenuation by
evaluating insulin sensitivity. These authors evaluated the effect of 7%
guar gum and 7% wheat bran on tissue specic and whole body insulin
sensitivity. One of the benets of reduced glycemia from guar gum
consumption is believed to be an enhancement in insulin sensitivity,
through less diurnal insulin production.
Cameron-Smith et al. (1997) found that bran fed rats consumed
more quantities of feed than guar fed rats. In streptozotocin (STZ)
induced diabetic rats, plasma glucose was reduced for guar fed rats
compared with those rats fed with bran. Hepatic glucose output was
higher in STZ diabetic rats, compared with a group of non-diabetic rats,
whichwere giventhe same diets. STZdiabetic rats fed withthe guar diet
had a signicantly lower basal glucose turnover, as well as an enhanced
metabolic clearance rate of glucose, compared with STZ diabetic rats
givena brandiet. Essentially, non-diabetic andSTZdiabetic rats fedwith
guar had improved insulin stimulated glucose production (less hepatic
glucose output) and clearance compared with non-diabetic and STZ
diabetic rats fed with bran.
STZ diabetic rats consuming the guar diet showed better glucose
utilisation in most tissues, with a statistical signicance seen in brown
adipose tissue, when compared with bran fed rats. In non-diabetic rats
the guar diet enhanced the glucose utilisation index in all tissues
measured except white adipose tissue. Tissues measured were the
soleus, red gastrocnemius, extensor digitorum longus, brain, brown
adipose tissue, heart and diaphragm. There was a statistical signicance
for the glucose utilisation index for the diaphragm and the red
gastrocnemius muscle between the guar and bran diets, with the guar
diet improving the glucose utilisation index.
Guar gumappeared to enhance the action of insulin and the proposed
mechanisms for this enhancement were 1) an attenuated postprandial
glycemia and insulinemia 2) the reduction or suppression of urinary
glucose loss, which may have restricted hyperphagia and 3) the viscosity
of the guar diet, which may also have restricted hyperphagia (Cameron-
Smith et al. 1997).
Suzuki and Hara (2004) also evaluated the effect of guar gum on
glycemia in rats. The guar gum hydrolysate (GGH) which has a low
viscosity was used. Rats were fed one of four diets 1) Dextrin 2) Dextrin
plus guar gum3) Fructose and 4) Fructose plus guar gum. Rats fed with
fructose only became glucose intolerant, while rats consuming fructose
withguar gumhad glucose area under the curve (AUC) values similar to
the dextrin fed groups. Glucose AUC at 060 min were 10.6, 9.88, 9.46
and 9.79 mmol/h/L for fructose, fructose plus guar gum, dextrin and
dextrinplus guar gumrespectively. Plasma insulinwas highest at 15and
30 min for the fructose fed group, while the insulin value was similar for
the other diet groups. Insulin AUC at 060 min were 0.54, 0.37, 0.34 and
0.29 mmol/h/L, for fructose, fructose plus guar gum, dextrin and dextrin
plus guar gum respectively. The fructose diet caused a reduction of the
glycogen concentration in the gastrocnemius muscle but consuming
guar gum alleviated this glycogen reduction.
Suzuki and Hara employed a lowviscosity guar gumin their study in
order to determine whether factors other than gastric emptying may be
responsiblefor glucoseattenuation. They proposedthat short chainfatty
acids were responsible for glucose attenuationseenwithsoluble dietary
bre and by extension that was seeninthis study. They did not consider
the halo effect, which may also contribute to blunted glycemia, as their
low viscosity gum may be coating the carbohydrate and thereby
depressinghydrolysis or digestion. Viscosity effects alonedonot seemto
account for the glycemia attenuating benets of guar gumconsumption
in animals.
Nunes and Malmlof (1992) evaluated the effects of guar gum and
cellulose on glucose absorption, insulin, gastric inhibitory peptide (GIP),
insulin-like growth factor 1 (IGF-1), as well as hepatic metabolism in
pigs. They found that the glucose attenuating effect of guar gumseemed
to be related to tempered digestion or absorption, but was not related to
reduced gastric emptying. In this experiment three catheters were
surgically placed into the portal vein, brachiocephalic artery and right
hepatic vein, while electromagnetic ow probes were situated around
theportal veinandhepatic artery. Threediets were administeredfor one
week each and comprised either a control, which contained 150 g/kg of
mica powder, a guar diet containing 60 g/kg guar and a diet with
150 g/kg puried cellulose. Each diet provided the same quantity of
starch and protein.
The guar gumdiet signicantly reduced glucose absorption without
altering the rate of hepatic glucose uptake and reduced insulin
production when compared to the mica and cellulose diets. Insulin
produced after consumption of the guar gum diet was 70% of that
produced after the mica only diet and 80% of the insulin produced in
relation to that seen with the cellulose diet. After consumption of guar
gumthe glucagon produced was 46%of that seen with the mica diet and
59% of the glucagon produced after consumption of the cellulose diet.
A similar trend was also seen with GIP where GIP produced after guar
consumptionwas 45%and56%of the quantityseenafter ingestionof the
mica only and cellulose diets respectively. Insulin-like growth factor-1
(IGF-1) production was also signicantly lower after ingestion of the
guar gum meal.
Nunes and Malmlof (1992) deduced the reduced quantity of
available carbohydrate for absorption, namely glucose caused the cascade
of events whereby less carbohydrate in the upper GI tract reduced GIP
release. This reduction inGIP was thought to have caused the reductionin
insulin secreted.
4. Rheological andphysiological effects of guar gumconsumptionin
human studies
Ellis, Apling, Leeds, and Bolster (1981) found bread supplemented
with 5%, 10% and 15% guar gum signicantly reduced serum insulin.
However, Groop, Aro, Stenman, and Groop (1993) suggested that in
humans guar gumconsumption caused an increase in insulin secretion,
based on their measurement of serum C-peptide and ascribed
enhanced hepatic extraction of insulin as the reason for reduced
seruminsulin levels. They studied the effects of consuming 15 g of guar
gum per day for 48 weeks by diet treated non-insulin dependent
diabetics. They found that guar gum moderately enhanced long term
glycemic control as well as postprandial glycemia.
Morgan, Tredger, Wright, and Marks (1990) looked at the effects of
10 g guar gum, 10 g sugar beet bre, 5 g glucomannan and 10 g soya
bean cotyledon bre on postprandial glycemia, insulin and gastric
inhibitory polypeptide (GIP) secretioninhealthypersons. Guar gumand
sugar beet bre signicantly reduced the AUC for glucose, compared
with the control meal at 690 mmol/L/min, 557 mmol/L/min and
589 mmol/L/minfor the control, guar andsugar beet meals respectively.
The AUC for insulin was signicantly reduced by the guar meal only at
3279 m U/L/min, while the control and sugar beet bre had values of
6528 mU/L/min and 6502 mU/L/min respectively. GIP response for the
time frame 090 minwas 919 g/L/minfor the control, 647 g/L/minfor
guar gum and 1138 g/L/min for sugar beet. Glucomannan and soya
cotyledon bre did not cause any change in postprandial glucose or GIP
on comparison with the control. Glucomannan caused a reduction in
insulin while soya bean bre caused an increase in the insulin response.
Morgan et al. (1990) also found an increase in liquid gastric
emptying, determined by circulating paracetamol levels, associated
withconsumptionof diets containingguar gumandsugar beet bre. The
composition of the test meal in this study was bread with honey and
1112 K.T. Roberts / Food Research International 44 (2011) 11091114
orange squash and the various types of bre. This high glucose
composition of the test meals may have affected gastric emptying.
Leclere et al. (1994) also found an increase in the ow rate for meals
with high glucose as opposed to high starch in their work.
Leclere et al. (1994) evaluated the effect of low viscosity guar gum
(LVGG) and high viscosity guar gum (HVGG) on the meal ow rate as
well as postprandial glycemia and insulinemia. This experiment also
evaluated the differences between LVGG and HVGG when paired with
glucose and starch. The meals consisted of HVGG plus glucose, HVGG
plus starch, LVGGplus glucose andLVGGplus starch. Whenthe viscosity
of the pairings was evaluated on a viscosimeter it was seen that ow
rates of meals containing glucose were signicantly higher than those
containing starch. Flow rates were 3.7 mm/s, 15.7 mm/s, 0.1 mm/s and
0.3 mm/s for HVGG plus glucose, LVGG plus glucose, HVGG plus starch
and LVGG plus starch respectively.
Meals with guar gum and starch were associated with slowed
gastric emptying due to viscosity while meals with glucose had no
viscosity effects. LVGG plus glucose and HVGG plus glucose gave similar
postprandial glucose responses, but HVGG plus glucose also gave
signicantly reduced postprandial insulin. LVGG plus starch gave
signicantly higher postprandial glucose thanHVGGplus starch. Morgan
et al. (1990) and Leclere et al. (1994) showed that the composition of
their meal may have affected viscosity and it may be possible that meals
with high levels of simple sugars as opposed to starch may play a part
not only in meal viscosity but gastric emptying. The drawback to this
experiment though was there were no controls. For example the glucose
diet without guar and the starch diet without guar, for comparison with
test meals.
Van Nieuwenhoven, Kovacs, Brummer, Westerterp-Plantenga, and
Brouns (2001) through a scintigraphic technique, showed there were
no signicant differences for gastric emptying or small intestinal transit
rate in humans, when guar gum was added to a semi-solid meal. The
semi-solid meal contained 0 g, 2.5 g, 3.5 g and 4.5 g of guar gum per
200 ml. When viscosity measurements were conducted on a rheometer
there were signicant differences between the control and 4.5 g of guar.
Therefore, an increase in viscosity in vitro did not correspond with a
reduction of gastric emptying or small intestinal transit in this study.
However, in this study the type of carbohydrate used in the semi-solid
meal was not stated. Van Nieuwenhoven et al. (2001) also stated that
the rate of gastric emptying is inuenced by meal volume, temperature
as well as the caloric contents.
The GI tract itself may cause changes to the viscosity of foods and
hence gastric emptying. These viscosity changes could be due to bolus
dilution via gastric secretions. The motility of the GI tract itself may
alsoplaya role inaltering viscosity bythe shear rate of the GI tract acting
on the non-Newtonian soluble bre. This means that as the bre is
exposed to an increase in shear stress the apparent viscosity of the
uid containing the bre will be reduced (Cameron-Smith et al., 1994;
Dikeman, Murphy & Fahey, 2006).
Wolever, Jenkins, Nineham, and Alberti (1979) found that 5 g guar
gum in bread and 5 g guar gum in soup signicantly reduced both
postprandial glucose and insulin, up to 120 min after consumption of
these products, when compared to their respective controls (no guar
gum). After consuming guar gumin soup the reduction in postprandial
glycemia and insulinemia was even more pronounced than that seen
fromconsuming bread with guar gum. It was proposed, this may be the
result of more complete hydration of the guar in the liquid soup, as
opposed to what may be incomplete guar hydration in semi-dry
products like bread. However, no actual tests were done to determine
the reason for these differences, for example no viscosity or hydration
measurements were conducted.
5. Conclusion
The effect of food matrix, rheology and composition on the
physiological effect of dietary bre is complicated and requires an
interdisciplinary approach. The harvesting conditions, purity and proces-
sing conditions for dietary bre are also just a fewfactors that may affect
rheology and physiological results in vitro and in vivo. According to
Morgan et al. (1990) the composition of a meal in itself is imperative
for the effect of dietary bre on gastric emptying. It is clear that the
mechanisms governing the physiological effects of dietary bre are both
complex and diverse, with even bres that are structurally similar
exhibiting varied outcomes for glucose tolerance, gastric emptying and
gut hormones.
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