KONJAC FLOUR
First draft prepared by P.J. Abbott
Food Science and Safety Section, National Food Authority, Canberra,
Australia
Explanation
Biological data
Biochemical aspects
Digestion in the small intestine
Fermentation in the large intestine
Human studies
Metabolism of fermentation end-products
Toxicological studies
Short-term toxicity
Long-term toxicity
Genotoxicity
Special studies: Nutrient absorption
Observations in humans
Vitamin absorption
Cholesterol absorption
Comments
Evaluation
References
1. EXPLANATION
Konjac flour was previously considered by the Committee at its
forty-first meeting (Annex 1, reference 107), when it allocated a
temporary ADI 'not specified' on the basis of the available data on
toxicology, particularly from human studies, the long history of use
of konjac as a food in China and Japan, and estimates of consumption
in traditional and anticipated uses. The results of additional
short-term studies of toxicity, which the Committee was informed had
been conducted in rats and dogs, together with adequate data on the
fate of konjac flour in the gut and information on its influence on
the bioavailability of fat-soluble vitamins were requested for review
by 1996.
At its present Meeting, the Committee considered some additional
data on the fate of konjac flour in the large intestine, including a
recent study with human faecal flora in vitro. The likely
fermentation end-products were also identified. Additional short-term
studies were considered, including a 28-day study on the effect of 10%
konjac flour on protein digestion and absorption in rats, and a
12-week study on the hypocholesterolaemic effects of konjac flour in
rats. The other short-term toxicity studies in rats and dogs referred
to previously (Annex 1, reference 107) were not available. An
additional long-term study in rats on the effects of konjac flour on
calcium and phosphorus metabolism and on tissue senescence was
considered. Two additional genotoxicity studies on konjac flour were
also available. With regard to the effect of konjac flour on the
availability of fat-soluble vitamins, data from studies in animals and
humans on the effect of konjac flour and other polysaccharide gums on
vitamin and cholesterol absorption were reviewed, and a rationale was
presented for a threshold dose for inhibition of absorption by konjac
flour.
2. BIOLOGICAL DATA
2.1 Biochemical aspects
Konjac flour is a high-relative-molecular-mass, linked, linear
copolymer of glucose and mannose ('glucomannan'), in which D-glucose
and D-mannose are linked by ß-1,4 glycosidic bonds in a molar ratio of
1:1.6. Branching from the C3 of either hexose is estimated to occur
every 10 repeating units through ß-1,3 linkages, and acetyl groups are
bound every 9-19 units, contributing to the high solubility of konjac
flour in water. Thus, while konjac flour is a polysaccharide gum, it
is considered to be soluble as a result of its ability to form a
solution of very high viscosity in water (Jenkins et al., 1986;
Nishinari et al., 1992).
2.1.1 Digestion in the small intestine
The indigestibility of konjac flour in the small intestine was
demonstrated in an experiment in which a pancreatic enzyme preparation
was unable to release glucose from konnyaku, a konjac flour
preparation (Inoue, 1942). There are no known digestive enzymes that
cleave the ß-1,4 linkages between the glucose and mannose units of the
polysaccharide backbone or the ß-1,3 linkages at the branch point. If
any acid or enzyme-catalysed hydrolysis occurs, the only breakdown
products would be D-glucose or D-mannose.
2.1.2 Fermentation in the large intestine
While there is no mammalian enzyme-catalysed hydrolysis of konjac
flour in the intestine, depolymerization to a variety of glucomanno-
oligosaccharides can occur in the large intestine as a result of the
action of intestinal microflora (Maeda, 1911; Inoue, 1942; Jenkins
et al., 1986). Enzymes with ß-mannanase and cellulase activities
which are capable of depolymerizing glucomannan have been detected in
a variety of microorganisms of different origins (Akino et al.,
1987; Yoshida & Morishita, 1991; Araki et al., 1992), including
faeces (Inoue & Inoue, 1956). The extent of depolymerization of
polysaccharide gums and the subsequent fermentation of monomers varies
widely. Some of the factors that influence the rate of digestion
include the nature of the fibre, the food in which it occurs, and the
presence of substances such as phytates, lectins, tannins, and
saponins, which appear to reduce fibre digestion (Jenkins et al.,
1986). The rat is considered to be a good experimental model for man
with regard to the fermentative breakdown and bulking capacity of
polysaccharide gums (Nyman et al., 1986). Direct evidence for the
degradation of polysaccharide gums in the intestine of humans was
provided by the studies of Vercellotti et al. (1978).
Potential fermentation of konjac flour by human faecal flora was
tested in vitro with a dilute suspension of bacteria prepared from
pooled human faeces. Konjac flour FW-KON (Lot no. 1294026; 83.4%
soluble polysaccharide gum) and control compounds were incubated with
faecal suspensions prepared from pooled samples provided by two
men and two women. The control compounds tested were D-glucose,
D-galactose, L-glucose, soluble starch, food-grade guar gum,
food-grade xanthan gum, food-grade sodium alginate, food-grade
carboxymethylcellulose, and food-grade pectin. Inoculated broths were
incubated for 0, 24, 48, and 96 h under anaerobic conditions at 37°C.
At the end of the incubation period, acid production was analysed with
a pH meter, and gas production was assessed by fluid displacement.
There was minimal fermentation of all compounds, none inducing a
decrease of one pH unit greater than the decrease observed in the
basal media. Statistical differences were, however, observed between
groups of compounds, although the data were not consistent. At 24 h,
the pH observed with D-glucose, D-galactose, soluble starch, pectin,
and guar gum was significantly lower than that with the basal medium.
At 48 h, significant differences were also seen with konjac flour and
xanthan gum, while with L-glucose, carboxymethylcellulose, and sodium
alginate the pH remained unchanged. At 96 h, the pH changes with
L-glucose, konjac flour, and carboxymethylcellulose were not
significant. Significantly elevated gas production was found at 24 h
in tubes containing D-galactose, soluble starch, konjac flour,
or guar gum. At 48 h, increased production was also seen with
D-glucose and pectin. At 96 h, all compounds except L-glucose,
carboxymethylcellulose, and sodium alginate produced significantly
more gas than the basal medium.
The level of fermentation of konjac flour appeared to be less
than that of D-glucose, D-galactose, soluble starch, pectin,
and guar gum but greater than that of xanthan gum, L-glucose,
carboxymethylcellulose, and sodium alginate (Carman et al., 1995).
2.1.3 Human studies
There have been no recent studies on the digestibility of konjac
flour in humans. Two older studies are reported below.
In a study to investigate the digestibility of konjac flour in
humans, one subject (the author) ate three pieces of konnyaku
containing about 20 g of glucomannan in his daily diet. The extent of
digestion was ascertained on the basis of the amount of sugar-
convertible carbohydrates excreted in the urine during consumption of
diets with and without konjac. The author reported that about 95% of
the konjac was digested, although how this occurred could not be
determined (Maeda, 1911).
In a second study, one subject ingested 30 g of konnyaku in the
form of a paste, with carmine as a non-absorbable marker. Faeces
collected during the two days after ingestion and those collected in a
subsequent two-day control period were analysed by hydrolysis with
hydrochloric acid and analysis for glucose. The unabsorbed
carbohydrate level was calculated from the difference in glucose
content between the two periods. The small difference in faecal
glucose content between the test and control periods led to the
conclusion that 99.5% of the ingested glucomannan had been fermented
in the large intestine. The fate of the digested konnyaku was not
established (Inoue, 1942).
2.1.4 Metabolism of fermentation end-products
The exact nature of the fermentation products of konjac flour has
not been identified. It is, however, reasonable to assume that
volatile (short-chain) fatty acids are the principal end-products of
microbial degradation, as for other indigestible polysaccharides (Yang
et al., 1970; Adiotomre et al., 1990). Some direct evidence that
volatile fatty acids are formed was provided in a study in rats fed
diets containing a sweetener, fructooligosaccharide, and in which
glucomannan was used for comparison. Both of these soluble,
indigestible polysaccharides resulted in increased faecal excretion of
acetate, propionate, butyrate, and isovalerate (Tokunaga et al.,
1986). There is ample evidence for the rapid, almost complete
absorption of short-chain fatty acids from the colon of humans (Dawson
et al., 1964; McNeil et al., 1978; Ruppin et al., 1980; Cummings
et al., 1987), rats (Remesy & Demigne, 1976), pigs (Argenzio &
Southworth, 1974), and dogs (Herschel et al., 1981).
Short-chain fatty acids (acetate, propionate, and butyrate) are
metabolized efficiently in humans. The concentrations were decreased
in portal, hepatic, and peripheral blood, and analysis of their molar
concentrations indicated greater uptake of butyrate by the colonic
epithelium and greater uptake of propionate by the liver (Vernay,
1987; Cummings et al., 1987). In a study in rats, the gut flora were
found to be the main source of acetate in the blood of normally fed
animals (Buckley & Williamson, 1977).
2.2 Toxicological studies
2.2.1 Short-term toxicity
In a study to investigate the digestion and absorption of
protein, groups of four male Sprague-Dawley rats were fed either 5%
cellulose (control), 10% cellulose, 10% pectin, or 10% konjac for 28
days. Body weights were recorded throughout the study, and urine and
faeces were collected. At the end of treatment, the rats were fasted
for 24 h and then fed 5 g/kg bw of brown rice and killed 5 h later.
The digestive system was segmented into stomach, upper and lower
portions of the small intestine, and large intestine, and the contents
of each were measured. The percent protein digested by each group was
assessed by measuring the nitrogen at intake and the levels in urine
and faeces.
Less protein was digested by rats fed konjac and pectin than
those fed cellulose, and the dry weight of the faeces of the pectin-
and konjac-fed rats was significantly lower than that of the
cellulose-fed rats. The weights of the contents of the different
segments of the digestive tract and the nitrogen contents of the
stomach and upper small intestine were similar in all groups, but the
nitrogen content of the large intestine was significantly greater in
rats fed pectin or konjac than in those fed cellulose. Konjac at a
dietary level of 10% thus decreased the digestion and absorption of
protein in the large intestine, with a consequent reduction in
body-weight gain. The study provides no indication of toxicity
resulting from intake of konjac (Miyoshi et al., 1987).
In a study to investigate the hypocholesterolaemic effects of
refined konjac meal containing about 80% glucomannan, groups of 12
five-week-old Sprague-Dawley rats of each sex were fed either a normal
basal diet, a hypercholesterolaemic diet (control diet containing 1%
cholesterol), or one of three test diets containing 2.5, 5, or 10%
refined konjac meal. Body weights were measured weekly. Four animals
of each sex from each group were killed after 4, 8, and 12 weeks of
treatment. Faeces were collected from all animals for three days
before sacrifice and were dried and weighed. Total cholesterol,
triglycerides, and high-density lipoprotein cholesterol were
determined in sera, and total cholesterol was measured in liver. The
iron, calcium, zinc, and copper contents of sera, femurs, and faeces
were also determined. Livers were obtained after sacrifice, and
sections were examined by light microscopy.
Body-weight gain was slightly but statisticaly significantly
lower in males fed 10% refined konjac meal than in the other groups
during the first eight weeks, probably due to the reduced food intake
in this group. Some rats in this group also had diarrhoea during this
period. Similar effects were not seen in the female rats. Dry faecal
weight was significantly greater for rats fed refined konjac meal than
for the other groups, demonstrating the ability of refined konjac meal
to increase stool bulk.
Serum cholesterol levels began to decrease after four weeks in
rats fed refined konjac meal at all doses, in comparison with the rats
receiving high cholesterol, but had returned to normal after 12 weeks.
The total cholesterol levels in the liver were significantly lower in
rats fed 10% refined konjac meal than in those fed 1% cholesterol at
four weeks. At 12 weeks, however, all treated groups showed reduced
total cholesterol in the liver in comparison with the high-cholesterol
control group.
Histological examination of the livers of rats fed 1% cholesterol
showed spreading fatty degeneration with focal necrosis and a non-
specific inflammation reaction. Similar changes were seen in the group
receiving refined konjac meal at the end of four weeks, but the
changes disappeared gradually with longer feeding times, and the
morphology of the liver was similar to that in the normal control
group at the end of 12 weeks. Changes were also observed on gross
examination of the liver. The authors suggested that the konjac flour
polysaccharide binds bile acids and depresses re-absorption in the
intestine, with a consequent reduction of lipid accumulation in the
liver. No differences in the mineral content of the sera or femurs
were seen between the groups at any time (Hou et al., 1990).
2.2.2 Long-term toxicity
In a study designed to investigate the effects of refined konjac
meal on calcium and phosphorus metabolism and on histopathology,
groups of 15 Sprague-Dawley rats of each sex were fed basal diet or
basal diet in which 1% of the cornstarch was replaced with refined
konjac flour, for 18 months. Body weights were measured weekly for
three months and monthly thereafter. At the end of treatment, the
animals were killed by bleeding from the femoral artery. Brain, liver,
aorta, kidney, spleen, and heart were removed and weighed and, in some
cases, examined by light and electron microscopy. The left femurs were
isolated and weighed, both fresh and dried, and the calcium and
phosphorus contents of the serum and femurs were determined.
Osteometry of the epiphyseal end of the left proximal tibia was also
perfomed, involving measurement of the trabecular volume, the mean
trabecular perimeter, the mean osteoid perimeter, the osteoid surface,
and cortical thickness. Blood samples were taken at three and nine
months to measure serum cholesterol.
Body-weight gain was similar in the two groups throughout the
study, and there was no difference in absolute or relative organ
weights or serum phosphorus and calcium levels between the control and
treated groups. The fresh and dried femur weights were similar in the
two groups, although there was a significant difference between the
sexes within each group. None of the osteometric parameters differed
significantly with treatment. Treated male rats had a statistically
significantly lower level of total cholesterol at nine and 18months
and a statistically significantly lower level of triglyceride at three
and nine but not at 18 months. Treated and control females had similar
total cholesterol levels, but triglyceride levels were lower in the
treated group at 18months. Electron microscopic examination of the
liver showed smaller, more lightly stained nuclei and reduced
bile-duct proliferation in the portal area in the treated rats. The
endothelial cells in the aorta of treated animals were smaller and
there was less thickening of the aortic wall. The authors concluded
that these changes were related to less senescence in the treated than
in the control group. There was no evidence of treatment-related
pathological changes.
The results thus indicate no significant effect of 1% refined
konjac meal on calcium or phosphorus metabolism or on bone structure;
however, treated animals had a lower level of blood lipids and fewer
signs of senescence in the cells of the brain, aorta, liver, and
heart. There was no evidence of toxicity. The NOAEL was 1% konjac
meal, equivalent to an intake of 500 mg/kg bw per day (Peng et al.,
1994, 1995; Zhang et al., 1994, 1995).
2.2.3 Genotoxicity
Konjac flour was tested for its ability to induce forward
mutations at the thymidine kinase (tk) locus in L5178Y tk+/-
lymphoma cells with and without microsomal activation (S9). As konjac
flour formed a cloudy suspension in dimethyl sulfoxide, this was
chosen as the vehicle; the flour was found to be insoluble at
concentrations of 125-1000 µg/ml. It was not cytotoxic in a 4-h assay
in the presence or absence of rat liver S9. Konjac flour did not
increase the mutation frequency in the presence or absence of S9
activation at concentrations of 7.81-1000 µg/ml or 15.6-997 µg/ml
(Cifone & Bowers, 1995)
Konjac flour was tested for its ability to induce micronuclei in
bone-marrow cells of groups of five CD-1 (ICR) mice of each sex, which
were given konjac flour suspended in corn oil by gavage at a dose of
5000 mg/kg bw and sacrificed 24, 48, or 96 h later. A second group of
mice were given deionized water and used as vehicle controls and, and
a third group given cyclophosphamide at 80 mg/kg bw were used as
positive controls and were sacrificed 24 h after treatment. The
numbers of micronuclei were recorded in polychromatic erythrocytes
from all animals; no increase in micronucleus formation was seen in
animals given konjac flour, but the positive controls had a
significant increase (Murli & Arriaga, 1995).
2.2.4 Special studies: Nutrient absorption
In a study to examine the hypocholesterolaemic effect of a series
of polysaccharide gums, groups of five male Wistar rats were fed diets
containing 5% of various gums, one of which was konnyaku powder
(konjac flour), and supplemented with cholesterol. Plasma and liver
cholesterol levels were examined after eight days and were found to be
significantly lowered in animals fed konjac flour (Kiriyama et al.,
1969). In a supplementary study, the hypocholesterolaemic activity of
konjac flour was shown to depend to some extent on its physical
characteristics, requiring that it be macromolecular and water-soluble
(Kiriyama et al., 1970).
A review of the in-vitro studies of Kiriyama and coworkers (1974)
(Annex 1, reference 108) suggested that konjac flour does not bind,
sequester, or adsorb bile acids since the equilibrium of bile acids
across a cellophane membrane in a single dialysis experiment was not
altered by the presence of konjac flour on one side of the membrane.
The results of another part of the study, on the effect of konjac
flour on bile-acid transport in everted sacs from rat ileum, confirmed
that rat ileum actively transports cholic and taurocholic acids and
showed that this transport is significantly inhibited by the presence
of 0.25%, but not by 0.05%, konjac flour in the outside medium. As
binding of konjac flour to the surface of the ileal sacs appeared to
be reversible, the inhibitory effect may be due to interference with
micelle formation by bile acids. The study provided some evidence that
there is a minimal inhibitory concentration of konjac flour in the
gastrointestinal medium. In the same experiment, when pectin was used
in the place of konjac flour, bile-acid transport was not inhibited at
concentrations of 0.05 or 0.5%, probably because of the lower
viscosity and water-holding capacity of pectin (Kiriyama et al.,
1974).
The interaction of bile acids with guar gum, konjac mannan, and
chitosan was compared in groups of male Wistar rats fed a meal
containing 5% of one of these polysaccharide gums; a control group was
fed a diet containing 5% cellulose (which is considered not to bind
bile acids or phospholipids in vivo). The animals were killed after
2 h, and the bile-acid content of the aqueous phase of the small
intestine was compared with the total content. The ratios were
considerably higher in animals fed guar gum or konjac mannan,
indicating binding by these fibres in the intestine, probably owing to
their very high viscosity at this concentration (Ebihara & Schneeman,
1989).
Pectin inhibited vitamin E absorption in rats during eight weeks'
feeding at levels of 6 and 8%, but not 3%, in the diet, again
suggesting a minimal inhibitory concentration (Schaus et al., 1985).
The results of these studies provide some evidence that konjac
flour can inhibit the transport of bile acids and absorption of
cholesterol at relatively high doses but not at lower doses.
2.3 Observations in humans
2.3.1 Vitamin absorption
The results of a study conducted by Doi and coworkers (1983) on
normal and diabetic subjects, reviewed previously (Annex 1, reference
108), suggested that viscous forms of polysaccharide gums, such as
konjac flour, may form a barrier around some fat-insoluble substances
(including glucose, essential electrolytes and cations, and possibly
vitamin B12), therefore delaying their absorption rather than
causing malabsorption. Because consumption of konjac flour may
interfere with the absorption of bile acids, however, the absorption
of the fat-soluble vitamin E, which depends on the presence of
conjugated bile acids, may also be impaired (Annex 1, reference 108).
The study of Doi et al. (1983) has a number of deficiencies, the
major one being that, although vitamin E and B12 levels were
measured up to 24 h after consumption of meals with and without 3.9 g
konjac flour, the serum vitamin E levelshad not returned to baseline
by this time, and thus the measurements were stopped too soon. The
possibility of delayed absorption rather than malabsorption of vitamin
E cannot be discounted on the basis of these data. As the serum levels
of bile acids were not measured in this experiment, a direct
correlation cannot be made between interference with bile-acid
absorption and reduced vitamin E absorption. The concentration of
konjac flour in the gastrointestinal tract during this experiment is
estimated to have been about 1%, on the basis of an intake of 400 g of
food during an average Japanese breakfast (Ito, 1988). The positive
results seen at this dose are consistent with a minimal inhibitory
concentration.
In a related study, the gel-forming gums pectin and guar gum were
shown to reduce the rate but not the overall level of absorption of
glucose and paracetamol, as measured by direct blood analysis in
healthy volunteers. The gums reduced peak absorption levels but
lengthened absorption (Holt et al., 1979).
The effect of konjac flour on the absorption of vitamin D was
measured in a double-blind trial on the efficacy of konjac flour
(identified as glucomannan) in the treatment of paediatric obesity.
The study involved 60 children under the age of 15 (mean age, 11.2
years; mean overweight, 46%). Thirty children received 1 g of
glucomannan twice daily for two months, and the other 30 children
received a placebo on the same schedule. The children received a
normal level of calories and were evaluated every two weeks for weight
changes in comparison with their initial weights. Clinical side-
effects were evaluated in both groups by measuring 25 indicators of
intestinal absorption, lipid metabolism, and thyroid and adenocortical
function, and the presence of clinical symptoms such as constipation,
diarrhoea, and abdominal pain. One of the parameters used to examine
intestinal absorption was serum vitamin D levels, which were measured
at the beginning and end of the study.
The two groups lost similar amounts of weight during the
two-month period, but the authors suggested that the decrease in
weight was due to continuous supervision. No significant differences
were found in intestinal absorption, thyroid or adenocortical
function, or clinical symptoms; however, significant differences were
found in lipid metabolism, the treated group having decreased
a-lipoprotein and increased pre-b-lipoprotein and triglyceride. Serum
vitamin D levels were similar in the two groups at the beginning and
end of the study (Vido et al., 1993).
2.3.2 Cholesterol absorption
In order to obtain a better understanding of the results of the
studies on vitamin absorption, the general properties of
polysaccharide gums, and specifically konjac flour, have been
considered. Two important properties of polysaccharide gums are their
ability to slow gastric emptying (Schwartz et al., 1982; Vahouny &
Cassidy, 1985) and to alter gastrointestinal transit times (Gohl &
Gohl, 1977; Schneeman, 1994). These characteristics are considered to
be related to the viscosity and water-holding capacity of these gums
(Eastwood et al., 1983; McBurney et al., 1985). Polysaccharide
gums influence the absorption of fat-soluble substances in two ways.
Firstly, they may cause an increase in the so-called 'unstirred layer'
or diffusion barrier on the mucosal surface (Vahouny & Cassidy, 1985;
Schneeman, 1994). Changes in the viscosity of this layer change its
apparent thickness (Anderson et al., 1989), and, because this layer
is rate-limiting in absorption, absorption rates from the intestine
are slowed and absorption along a greater length of the gut is
promoted (Schneeman, 1994). Secondly, polysaccharide gums may reduce
the level of enterohepatic circulation of bile acids and thus
interfere with bile-acid emulsification of fatty substances
(Vahouny & Cassidy, 1985). Whatever the mechanism, dietary intake of
polysaccharide gums, including konjac flour, lowers the serum levels
of fat-soluble substances such as cholesterol. Thus, studies on the
effect of konjac flour on serum cholesterol may be indicative of
effects on other fat-soluble substances such as vitamins.
The results of a clinical study by Zhang and coworkers (1990),
designed to examine the effect of daily consumption of foods
containing 5 g konjac flour on lipid metabolism, were reviewed
previously (Annex 1, reference 108). At the end of the 44 days of
treatment, total serum cholesterol, triglycerides, and low-density
lipoprotein levels were significantly reduced and that of high-density
lipoprotein was significantly increased in the treated group as
compared with the controls. After the 45-day recovery period, however,
there were no differences in these parameters between the groups.
The results of a clinical study by Huang et al. (1990), which
was designed principally to examine the effects of konjac flour on
blood glucose levels in 72 diabetic patients over a 65-day period,
were also reviewed previously (Annex 1, reference 108). Overall, the
study did not indicate that 2% konjac flour in the diet lowers blood
lipid levels, except in 13 subjects with hyper-triglyceridaemia in
whom triglyceride levels were significantly decreased.
The results of these two studies suggest that the effect of
konjac flour on blood cholesterol levels is dose-dependent and perhaps
reversible.
3. COMMENTS
The Committee reviewed data from additional short-term studies
and a long-term toxicity study, all conducted in rats. The short-term
studies were a 28-day study on the effect of konjac flour on
protein digestion and absorption and a 12-week study on the
hypocholesterolaemic effect of konjac flour. The additional long-term
study in rats addressed the effect of konjac flour on calcium and
phosphorus metabolism and histopathology. While these studies were not
specifically designed to assess the potential toxicity of konjac
flour, no evidence of toxicity was reported with 10% in the diet for
up to 12 weeks or with 1% in the diet for 18 months. Two additional
studies on genotoxicity provided no evidence of potential to induce
forward mutations at the thymidine kinase locus in cells in culture or
to induce micronuclei in mouse bone marrow. The Committee also
considered some additional data on the fate of konjac flour in the
large intestine, including a recent study of human faecal flora
in vitro, which showed that extensive hydrolysis of konjac flour
occurs in the large intestine. Konjac flour underwent less
fermentation than D-glucose, D-galactose, soluble starch, pectin, and
guar gum but more than xanthan gum, L-glucose, carboxymethyl-
cellulose, and sodium alginate. Although only indirect evidence was
provided, the Committee concluded that konjac flour, like other
polysaccharide gums, undergoes fermentation in the large intestine to
fatty acids (acetate, propionate, and butyrate).
The Committee reviewed data from studies in animals and humans
on the effect of konjac flour and other polysaccharide gums on the
absorption of fat-soluble vitamins and cholesterol and the
re-absorption of bile acids. The available data indicate that konjac
flour affects the absorption of vitamin E and cholesterol only at high
doses (possibly through interference with bile-acid micelle formation
and subsequent interference with transport mechanisms). The Committee
noted that there were still no definitive studies to establish the
threshold dose of konjac flour that affects vitamin E absorption but
considered that it was likely to be much higher than the levels of
intake of konjac flour when used as a food additive.
4. EVALUATION
The Committee stressed that its evaluation applies only to the
use of konjac flour as a food additive. The Committee concluded that
the additional studies provided no evidence of adverse effects
attributable to konjac flour in experimental animals. Metabolically,
konjac flour behaves in the intestine in a similar way to other
polysaccharide gums. On the basis of this re-assessment and on the
anticipated levels of use as a food additive (as a thickener,
emulsifier, stabilizer, gelling agent, texturizer, and glazing agent),
the Committee established an ADI 'not specified' for konjac flour.
5. REFERENCES
Adiotomre, J., Eastwood, M.A., Edwards, C.A. & Brydon, W.G. (1990)
Dietary fiber: in vitro methods that anticipate nutrition and
metabolic activity in humans. Am. J. Clin. Nutr., 52, 128-134.
Akino, T., Nakamura, N. & Horikoshi, K. (1987) Production of
ß-mannosidase and ß-mannanase by an Alkalophilic bacillus sp.
Appl. Microbiol. Biotechnol., 26, 323-327.
Anderson, B.W., Kneip, J.M., Levine, A.S. & Levitt, M.D. (1989)
Influence of infusate viscosity on intestinal absorption in the rat.
Gastroenterology, 97, 938-943.
Araki, T., Tamaru, Y. & Morishita, T. (1992) ß-1,4-Mannanases from
marine bacteria, Vibrio spp. MA-129 and MA-138 J. Gen. Appl.
Microbiol., 38, 343-351.
Argenzio, R.A. & Southworth, M. (1974) Sites of organic acid
production and absorption in gastrointestinal tract of the pig.
Am. J. Physiol., 228, 454-460.
Buckley, B.M. & Williamson, D.H. (1977) Origin of blood acetate in the
rat. Biochem. J., 166, 539-545.
Carman, R.J., Kotkoskic, L.A. & Evans, D.T. (1995) In vitro
fermentation of konjac flour FW-KON by human fecal flora. Unpublished
study (FMC Report No. 194-1976) from TechLab. Inc., Blacksburg,
Virginia, USA. Submitted to WHO by FMC Corporation, Princeton, New
Jersey, USA.
Cifone, M.A. & Bowers, L. (1995) Mutagenicity test on konjac flour
FW-KON in the L5178Y TK+/- mouse lymphoma forward mutation assay with
a confirmatory assay. Unpublished study (FMC Report No. 195-1979) from
Corning Hazleton, Vienna, Virginia, USA. Submitted to WHO by FMC
Corporation, Princeton, New Jersey, USA.
Cummings, J.H., Pomare, E.W., Branch, W.J., Naylor, C.P.E. &
MacFarlane, G.T. (1987) Short chain fatty acids in human large
intestine, portal, hepatic and venous blood. Gut, 28, 1221-1227.
Dawson, A.M., Holdsworth, C.D. & Webb, J. (1964) Absorption of short
chain fatty acids in man. Proc. Soc. Exp. Biol. Med., 117, 97-100.
Doi, K., Matsuura, M., Kawara, A., Tanaka, T. & Baba, S. (1983)
Influence of dietary fiber (konjac mannan) on absorption of vitamin
B12 and vitamin E. Tohoku J. Exp. Med., 141 (Suppl.), 677-681.
Eastwood, M.A., Robertson, J.A., Brydon, W.G. & MacDonald, D. (1983)
Measurement of water-holding properties of fibres and their faecal
bulking ability in man. Br. J. Nutr., 50, 539-547.
Ebihara, K. & Schneeman, B.O. (1989) Interaction of bile acids,
phospholipids, cholesterol and triglyceride with dietary fibers in the
small intestine of rats. J. Nutr., 119, 1100-1106.
Gohl, B. & Gohl, I. (1977) The effect of viscous substances on the
transit time of barley digesta in rats. J. Sci. Food Agric., 28,
911-915.
Herschel, D.A., Argenzio, R.A., Southworth, M. & Stevens, C.E. (1981)
Absorption of volatile fatty acid, Na, and H2O by the colon of the
dog. Am. J. Vet. Res., 42, 1118-1124.
Holt, S., Carter, D.C., Heading, R.C., Prescott, L.F. & Tothill, P.
(1979) Effect of gel fibre on gastric emptying and absorption of
glucose and paracetamol. Lancet, i, 636-639.
Hou, Y.-H., Zhang, L.-S., Zhou, H.-M., Wang, R.-S. & Zhang, Y.-Z.
(1990) Influences of refined konjac meal on the levels of tissue
lipids and the absorption of four minerals in rats. Biomed. Environ.
Sci., 3, 306-314.
Huang, C.-Y., Zhang, M.-Y., Peng, S.-S., Hong, J.-R., Wang, X., Jiang,
H., Zhang, F., Bai, Y., Liang, J., Yu, Y., Luo, Z., Zhang, X. & Zhou,
Z. (1990) Effect of konjac food on blood glucose level in patients
with diabetes. Biomed. Environ. Sci., 3, 123-131.
Inoue, M. (1942) Studies on enteric bacteria associated with digestion
of konnyaku mannan. Eiyogaku Zasshi, 2 (Suppl.), 9-18.
Inoue, N. & Inoue, K. (1956) Aerobacter type bacteria associated with
digestion of konnyaku mannan. J. Ferm. Technol., 34, 271-281.
Ito, Y., ed. (1988) Daily Intakes of Food Additives in Japan--
Determination of Food Additive Residues in Food (1976-1985), Tokyo,
Ministry of Health and Welfare, Food Chemistry Division.
Jenkins, D.J.A., Jenkins, A.L. Wolever, T.M.S., Rao, A.V. & Thompson,
L.U. (1986) Fiber and starchy foods: Gut function and implications in
disease. Am. J. Gastroenterol., 81, 920-930.
Kiriyama, S., Okazaki, Y. & Yoshida, A. (1969) Hypocholesterolemic
effect of polysaccharides and polysaccharide-rich foodstuffs in
cholesterol-fed rats. J. Nutr., 97, 382-388.
Kiriyama, S., Morisaki, H. & Yoshida, A. (1970) Changes in
hypocholesterolemic activity in rats by various konnyaku powder
treatments. Agr. Biol. Chem., 34, 641-643.
Kiriyama, S., Enishi, A. & Yura, K. (1974) Inhibitory effect of konjac
mannan on bile acid transport in the everted sacs from rat ileum.
J. Nutr., 104, 69-78.
Maeda, M. (1911) Physiological study of konnyaku (part 1). Tokyo
Igaku Kaishi, 25, 518-525.
McBurney, M.I., Horvath, P.J., Jeraci, J.L. & van Soest, P.J. (1985)
Effect of in vitro fermentation using human faecal inoculum on the
water-holding capacity of dietary fibre. Br. J. Nutr., 53, 17-24.
McNeil, N.I., Cummings, J.H. & James, W.P.T. (1978) Short chain fatty
acid absorption by the human large intestine. Gut, 19, 819-822.
Miyoshi, H., Okuda, T., Ishi, K., Ohsuga, Y., Tomeda, M. & Koishi, H.
(1987) The effects of cellulose, pectin and konjac intake on growth
and digestibility in rats. Osaka-Shiritsu Daigaku Seikatsulkaoakubu
Kiyo, 35, 23-28.
Murli, H. & Arriaga, J. (1995) Mutagenicity test on konjac flour
FW-KON in an in vivo mouse miconucleus assay. Unpublished study (FMC
No. 195-1980) from Corning Hazleton, Vienna, Virginia, USA. Submitted
to WHO by FMC Corporation, Princeton, New Jersey, USA.
Nishinari, K., Williams, P.A. & Phillips, G.O. (1992) Review of the
physicochemical characteristics and properties of konjac mannan.
Food Hydrocolloids, 6, 199-222.
Nyman, M., Asp, N.-G., Cummings, J. & Wiggins, H. (1986) Fermentation
of dietary fibre in the intestinal tract: Comparison between man and
rat. Br. J. Nutr., 55, 487-496.
Peng, S.-S., Zhang, M.-Y., Zhang, Y.-Z. & Wu, Z.-H. (1994) Effect of
refined konjac meal on cell aging of brain liver and cardiovascular
tissue in rats. Yingyang Xuebao, 16, 280-284.
Peng, S.-S., Zhang, M.-Y., Zhang, Y.-Z. & Wu, Z.-H. (1995) Long-term
animal feeding trial of the refined konjac meal. II. Effects of the
refined konjac meal on the aging of the brain, liver and
cardiovascular tissue cells in rats. Biomed. Environ. Sci., 8,
80-87.
Remesy, C. & Demigne, C. (1976) Partition and absorption of volatile
fatty acids in the alimentary canal of the rat. Ann. Rech. Vet., 7,
39-55.
Ruppin, H., Bar-Meir, S., Soergel, K.H., Wood, C.M. & Schmitt,
M.G. Jr (1980) Absorption of short-chain fatty acids by the colon.
Gastroenterology, 78, 1500-1507.
Schaus, E.E., Delumen, B.O., Chow, F.I. Reyes, P. & Omaye, S.T. (1985)
Bioavailability of vitamin E in rats fed graded levels of pectin.
J. Nutr., 115, 263-270.
Schneeman, B.O. (1994) Carbohydrates: Significance for energy balance
and gastrointestinal function. J. Nutr., 124 (Suppl.), 1747S-1753S.
Schwartz, S.E., Levine, R.A., Singh, A., Scheidecker, J.R. & Track,
N.S. (1982) Sustained pectin ingestion delays gastric emptying.
Gastroenterology, 83, 812-817.
Tokunaga, T., Oku, T. & Hosoya, N. (1986) Influence of chronic intake
of new sweetener fructooligosaccharide (Neosugar) on growth and
gastrointestinal function of the rat. J. Nutr. Sci. Vitaminol., 32,
111-121.
Vahouny, G.V. & Cassidy, M.M. (1985) Dietary fibers and absorption of
nutrients. Proc. Soc. Exp. Biol. Med., 180, 432-446.
Vercellotti, J.R., Salyers, A.A. & Wilkins, T.D. (1978) Complex
carbohydrate breakdown in the human colon. Am. J. Clin. Nutr., 31,
S86-S89.
Vernay, M. (1987) Effects of plasma aldosterone on butyrate absorption
and metabolism in the rabbit proximal colon. Comp. Biochem. Physiol.,
86A, 657-662.
Vido, L., Facchin, P., Antonello, I., Gobber, D. & Rigon, F. (1993)
Childhood obesity treatment: Double blinded trial on dietary fibres
(glucomannan) versus placebo. Paediatr. Paedol., 28, 133-136.
Yang, M.G., Manoharan, K. & Mickelsen, O. (1970) Nutritional
contribution of volatile fatty acids from the cecum of rats.
J. Nutr., 100, 545-550.
Yoshida, S. & Morishita, H. (1991) Biodegradation of sodium
carboxymethyl cellulose and glucomannan by microorganisms from soils.
J. Antibact. Antifungal Agents, 19, 105-110.
Zhang, M.-Y., Huang, C.-Y., Hong, J.-R. & Peng, S.-S. (1990) The
effect of foods containing refined konjac meal on human lipid
metabolism. Biomed. Environ. Sci., 3, 99-105.
Zhang, M.-Y., Peng, S.-S., Zhang, Y.-Z. & Wu, Z.-H. (1994) Effects of
refined konjac meal on calcium and phosphorus metabolism and bone in
rats. Yingyang Xuebao, 16, 160-163.
Zhang, M.-Y., Peng, S.-S., Zhang, Y.-Z. & Wu, Z.-H. (1995) Long-term
animal feeding trial of the refined konjac meal. I. Effects of the
refined konjac meal on the calcium and phosphorus metabolism and the
bone in rat. Biomed. Environ. Sci., 8, 74-79.
See Also:
Toxicological Abbreviations
Konjac flour (WHO Food Additives Series 32)
KONJAC FLOUR (JECFA Evaluation)