KONJAC FLOUR
First draft prepared by
Dr K. B. Ekelman and Dr G. A. Dannan, Additives Evaluation Branch
Division of Health Effects Evaluation
Center for Food Safety and Applied Nutrition
Food and Drug Administration, Washington, DC, USA
1. EXPLANATION
Konjac flour, commonly referred to as konjac mannan, is a
ß-D-(1->4)-linked linear copolymer of glucose and mannose
substituted with O-acetate every 9-19 sugar units. Konjac flour
is derived from the tubers of Amorphophallus konjac. The flour,
which constitutes 60-80% of the dried root tuber, is obtained by a
dry milling process of thin tuber slices. Carbohydrates (as water-
soluble fiber) make up approximately 75% of konjac flour, the
remainder being protein (2-8%), fat (<1%), ash (3-5%), and moisture
(<15%).
Konjac flour has not been evaluated previously by the
Committee. The current evaluation was undertaken because of
anticipated new food additive uses of konjac flour as a gelling
agent, thickener, emulsifier, and stabilizer in such foods as soup,
gravy, mayonnaise, and jam. Nevertheless, there is a long history
of use of konjac (containing approximately 4% konjac flour) in
traditional Japanese and Chinese foods; the average consumption of
konjac flour from these uses is estimated to be 2-3 g/person/day,
and occasionally as high as 4 g/person/day. The anticipated maximum
consumption of konjac flour from food additive uses is about
3 g/person/day.
Numerous physicochemical studies have been done on konjac. The
primary polysaccharide constituent in konjac flour is a high-
molecular-weight glucomannan (200 000 to 2 000 000 daltons depending
on the strain and place of cultivation) in which D-glucose and
D-mannose, in a molar ratio of 1.0:1.6, are linked by ß-1->4
glycosidic bonds. Branching from the C3 of either hexose is
estimated to occur every ten repeating units through 1,3 linkages.
Acetyl groups bound every 9-19 units along the glucomannan backbone
are thought to contribute to the high solubility characteristic of
konjac flour (Nishinari et al., 1992).
Doi and coworkers (1982) reported that the viscosity of konjac
flour is greater than that of guar gum, one of the most viscous of
the dietary fibers. Ebihara and coworkers (1981) reported that,
compared to dietary fibers such as carboxymethylcellulose (CMC) and
pectin, the relative viscosity of konjac flour increases
extraordinarily as its concentration in water increases. When fiber
concentration in water is increased from 1 to 3 g/l, the relative
viscosity of pectin increases from 1.8 to 3.2, the relative
viscosity of CMC increases from 4.6 to 10.4, and the relative
viscosity of konjac flour increases from 5.7 to 171.2 (water was
arbitrarily assigned a viscosity of 1.0).
2. BIOLOGICAL DATA
2.1 Biochemical aspects
Due to the ß-glycosidic linkages between the glucose and
mannose building blocks (ß-1->4 linkages in the main chain and
ß-1->3 linkages at the branch points) konjac flour is commonly
regarded as a non-digestible polysaccharide. Because of its high
water solubility, conferred mainly by attached acetyl groups, konjac
flour is also classified as a soluble fiber. Following alkali
treatment or heating, konjac flour loses acetyl groups and forms a
gel. Gelling is thought to result from cross-linking, mainly
through hydrogen-bonding between konjac flour moieties that are
deficient in acetyl groups (Nishinari et al., 1992).
Since konjac flour's polymeric structure is assumed to render
it unavailable for intestinal degradation or absorption, konjac
flour is commonly believed to pass through the gastrointestinal
tract unaltered. Although no studies have been performed for
evaluating the possible degradation or hydrolysis of konjac flour in
the intestinal tract, formation of oligo- and mono-saccharides from
konjac flour has been observed in the presence of 1N sulfuric acid
at 100°C (Japan Food Research Laboratories, 1984).
2.2 Toxicological studies
2.2.1 Acute toxicity studies
Table 1 summarizes the results of acute toxicity studies with konjac flour:
Table 1. Acute toxicity studies with konjac flour
Species Sex Route LD50 Reference
Mouse M & F oral1 >2800 mg/kg bw Oketani et al., 1984
Rat M & F oral2 >5 000 mg/kg bw3 Kotkoskie et al., 1992
Rat M & F inhalation2 >0.0015 mg/l Kotkoskie et al., 1992
Rabbit M & F dermal2 >2 000 mg/kg bw Kotkoskie et al., 1992
(1) Test substance was identified as konjac mannan.
(2) Test substance was identified as konjac flour.
(3) This was the only dose tested.
2.2.2 Short-term toxicity studies
In a study conducted to determine appropriate doses for a
subsequent embryotoxicity study, Burger and coworkers (1992) fed
diets containing 2% carob gum (controls) or 2% konjac flour (Test
substance identified as konjac flour from Amorphophallus
oncophyllus from Thailand) to two groups of 15 adult female
British domestic short-hair cats for eight weeks. Feed consumption
and body weight were monitored throughout the study. Although no
data were presented, report stated that both diets had digestibility
coefficients similar to typical canned cat foods. In addition, body
weights of cats fed diets containing 2% konjac flour increased more
than body weights of cats fed the control diet during the study.
Mean body weight gain in adult female cats during the 8-week period
was 59±3 g/wk for controls (2% carob gum) and 86±5 g/wk for konjac
flour-fed cats; however, the respective mean feed consumption was
190±8 g/day and 181±12 g/day (Burger et al., 1992).
2.2.3 Long-term toxicity/carcinogenicity studies
No information was available.
2.2.4 Reproduction studies
No information was available.
2.2.5 Special studies on anti-carcinogenic effects
A diet containing refined konjac was evaluated for its effects
on the incidence of spontaneous liver tumours in C3H/He mice; these
tumours generally occur in 60-70% of one-year-old mice of this
strain. At seven weeks of age, groups of 30 male mice were fed
either a powdered commercial diet (control group) or the same diet
to which 10% konjac flour (identified as konjac mannan) had been
added (konjac flour group). At one year of age, all animals were
necropsied and the number and size of liver tumour nodules were
determined. There was a slight decrease in the number of animals
with liver tumours in the konjac flour group (control: 63% of 24
mice; konjac flour: 48% of 23 mice) and a statistically significant
decrease (p<0.05) in the mean number of tumour nodules per mouse in
the konjac flour group (control: 1.1; konjac flour: 0.5). However,
mean tumour size was not altered. Weight gain in the 10% konjac
flour diet group was lower (p<0.05) than that in the control diet
group throughout the experiment, but there was no change in total
feed intake between the control and konjac flour-treated mice.
While feed efficiency was decreased in konjac flour-treated mice
compared to controls (control: 2.9%; konjac flour: 2.3%), the
decrease was not statistically significant. In this study,
spontaneous liver tumours in C3H/He mice were inhibited by
maintaining the mice on a diet containing 10% konjac flour, although
the reviewers note that animals maintained on this diet consumed
approximately 10% fewer calories per day than control animals
(Mizutani and Mitsuoka, 1982).
In another study by the same authors the effect of a diet
containing 5% konjac flour on the incidence of colon tumours induced
by 1,2-dimethylhydrazine (DMH) in rats was studied. Five-week old
male Fisher 344 rats (20/group) were fed either a commercial diet
(414 kcal/100 g) or a similar diet containing 5% konjac flour
(identified as konjac mannan, diet had an energy content of 393
kcal/100 g). At six weeks of age, and weekly thereafter for a total
of 13 weeks, all rats were injected i.p. with 20 mg DMH/kg bw. Feed
consumption was measured weekly for 20 weeks (duration of the study
was approximately 27 weeks). Rats were necropsied 13 weeks after
the last injection of DMH; the intestine (small and large) and other
organs (unspecified) were examined grossly and microscopically for
numbers and types of tumours. Throughout the study, body weights of
konjac flour-fed rats were significantly lower than those of rats
fed the control diet; however, there was no significant difference
in feed efficiency between konjac flour-fed and control rats. The
incidence of DMH-induced colon tumours was significantly lower in
the konjac flour-fed group (39%) compared to the control group
(75%). The number of colon adenocarcinomas per rat was also
significantly lower in konjac flour-fed rats (0.22) than in control
rats (0.75). However, the mean diameter of colon tumours was not
significantly different in the two groups of rats (konjac flour-fed
rats: 5.8±1.3 mm; control rats: 6.9±3.6 mm).
In contrast to the effects reported for colon tumours, dietary
konjac flour had no significant effect on the incidence of tumours
of the small intestine, all of which were adenocarcinomas in this
study (control: 45%; konjac flour: 33%); mean diameters of
adenocarcinomas of the small intestine were not significantly
different in the two groups (control: 8±4 mm; konjac flour: 6±2 mm).
Dietary konjac flour did not appear to have a significant effect on
the incidences of ear duct or pancreas tumours in rats in this study
(Mizutani and Mitsuoka, 1983).
2.2.6. Special studies on embryotoxicity
Pregnant British short-hair domestic cats were fed diets
containing 2% carob gum (9 control cats) or 2% konjac flour (6 cats;
test substance identified as konjac flour from Amorphophallus
oncophyllus from Thailand) during gestation. Body weights were
recorded weekly until parturition and feed consumption was recorded
daily during the week prior to parturition. Actual intake of konjac
flour during the week prior to parturition ranged from 0.98 to
3.08 mg/kg bw/day. All pregnant females completed a normal
gestation period and that there were no significant differences in
body weight changes of females fed control and konjac flour-
containing diets. Mean birth weight of kittens born to control cats
was statistically significantly lower (p<0.01) than mean birth
weight of kittens born to konjac flour-fed cats, but mean litter
size for control cats was less than mean litter size for konjac
flour-fed cats: A total of 32 kittens (mean birth weight 104±17 g)
were born to 9 control cats and 36 kittens (mean birth weight
95 g±22 g) were born to 6 konjac flour-fed cats; mean litter size
was 3.5±1.6 for controls and 5.1±1.2 for konjac flour-fed cats (mean
control litter size for cats in the same colony was reported to be
3.3±1.5). All cats in the study completed lactation and reared
their progeny successfully. The study also reported that
biochemical and haematological parameters were within normal ranges
throughout the study (no data were provided) (Burger et al.,
1992).
2.2.7 Special studies on gastrointestinal effects.
There was no change in total faecal microflora count in 30 male
C3H/He mice fed a diet containing 10% konjac flour (test substance
was identified as konjac mannan) for one year compared to 30 male
mice fed a powdered control diet. Of the 11 specific types of
microflora that were examined, however, two were significantly
changed: the frequency of bifidobacteria increased from 30% in
control mice to 100% in konjac flour-fed mice and the log count of
enterobacteriaceae increased from 6.0 in control mice to 6.6 in
konjac flour-fed mice (Mizutani and Mitsuoka 1982).
Five-week-old male C3H/He mice bearing human flora were either
maintained on a control diet or fed a diet containing 10% konjac
flour (test substance was identified as konjac mannan, sterilized by
gamma-radiation from 60Co). When the mice were five months old,
microflora, enzymes, and putrefactive products were analyzed in
faecal samples from animals in the control and konjac flour-fed
groups. Total bacterial counts were nearly identical in control and
konjac flour-fed mice; however, streptococcus bacteria were
significantly reduced in the konjac flour-fed mice. Of the soluble
enzymes measured, ß-glucuronidase and nitroreductase activities were
significantly reduced in the konjac flour-fed mice (67% and 19% of
activities in control mice, respectively) while azoreductase
activity was slightly increased (139% of activity in control mice).
Several putrefactive metabolites (p-cresol, indole, and skatole)
were decreased in konjac flour-fed mice compared to control mice.
Dietary konjac flour, through material sequestration and lowering of
substrate concentration, might lead to suppression of bacterial
enzyme activities and intestinal metabolism without significantly
affecting microflora composition (Fujiwara et al., 1991).
Three-month-old Fisher 344 male rats were switched from a basal
diet to a similar diet containing 10% konjac flour (test substance
was identified as konjac mannan, sterilized by gamma-radiation from
60Co), to which they were allowed ad libitum access for two
months. Soluble enzyme activities were measured in fresh faecal
samples collected two days before and 19, 29, and 39 days after rats
were placed on the 10% konjac flour diet. Putrefactive products
were analyzed in fresh faecal samples collected the day before and
on days 20, 30, and 40 after rats were placed on the konjac flour
diet. Mean faecal ß-glucuronidase activity (n = 13 rats) initially
rose, then decreased significantly to approximately one-third of its
original level of activity at the end of the experimental period.
Two faecal reducing enzyme activities significantly decreased
following introduction of the konjac flour diet: nitroreductase
activity was decreased approximately 2-fold and azoreductase
activity was decreased approximately 5-fold by the end of the study.
As well, the gastrointestinal (microflora) metabolites tyrosine and
tryptophan were significantly altered in rats that consumed a konjac
flour-containing diet for 2 months. The reviewers note that
concurrent control animals were not included in this study, and
effects attributed to consumption of konjac flour could also be due
to factors such as age or changes in the test animals' environment
(Fujiwara et al., 1991).
Groups of weanling male Wistar rats (six/group) were fed a
basal diet (control group: 67% corn starch, 21% casein, 7% corn oil,
4% salt mix and 1% vitamins) or diets containing 20% konjac flour or
20% cellulose (test diets were prepared by substituting the test
substance for an equal weight of corn starch in the basal diet,
konjac flour was identified as having been derived from
Amorphophallus konjac. After eight weeks, total protein, DNA,
RNA, and the activity of (Na+K)ATPase were determined in homogenates
of caecal and colonic mucosa. Compared to rats fed the basal diet,
feed intake of the konjac flour-fed rats was unchanged but feed
intake of the cellulose-fed rats was significantly increased (data
not shown). After eight weeks, the konjac flour-fed group had a
significantly reduced mean body weight (90% of control); wet weights
of the caecum and colon in konjac flour-fed rats were significantly
increased compared to control rats (approximately 300% and 25%,
respectively). In contrast, the average body weight of cellulose-
fed rats was not significantly different from control rats, but wet
weights of the caecum and colon in cellulose-fed rats were increased
by approximately 25% and 60%, respectively. Total mucosal DNA in
the caecum and colon of konjac flour-fed rats was significantly
increased compared to control rats (263% and 159%, respectively);
total mucosal DNA in the caecum and colon of cellulose-fed rats was
also increased compared to control rats (148% and 187%,
respectively). Ratios of mucosal RNA/DNA and protein/DNA in the
caecum were significantly increased in konjac flour-fed rats
compared to control rats. Caecal and colonic mucosal (Na+K)ATPase
activities (expressed per mg protein) were significantly increased
in konjac flour- or cellulose-fed rats compared to control rats;
konjac flour-fed rats had a greater increase in mucosal ATPase
activity in the caecum than in the colon (180% vs. 150%,
respectively) while the opposite was true for cellulose-fed rats
(150% vs. 219%, respectively). Based on these results, this report
suggests that caecal enlargement in rats due to ingestion of konjac
flour results from both increased number (hyperplasia) and size
(hypertrophy) of mucosal cells, but that colonic enlargement due to
ingestion of konjac flour and colonic and caecal enlargement due to
ingestion results from hyperplasia only (Konishi et al., 1984).
2.2.8 Special studies on genotoxicity
Konjac flour was non-mutagenic in five tester strains (TA98,
TA100, TA1535, TA1537, and TA1538) of Salmonella typhimurium in
the presence or absence of liver microsomal metabolic activation
(Kotkoskie et al., 1992).
2.2.9 Special studies on lipid metabolism
Venter and coworkers (1990) studied the effect of konjac flour
on plasma fibrinogen, serum and liver lipid, glucose tolerance,
insulin response, and liver glycogen in baboons fed a "Western"
diet. Twelve male baboons (mean weight of 19±3 kg) were fed a
"Western" diet (approximately 400 g/day) with or without konjac
flour (5%) or sodium propionate (2%) supplements for periods of 9
weeks in a crossover, randomized order with period of stabilization
between treatment periods. The "Western" diet consisted of 38.3 g
corn meal, 13.4 g beef tallow, 10 g sucrose, and 38.3 g of a
commercially prepared dietary supplement containing protein,
vitamins, and minerals per 100 g diet (the supplement results in
normal growth and excellent health when fed in combination with corn
meal to young baboons). Parameters were measured before and 4 and 9
weeks after the beginning of each treatment period. After 9 weeks,
serum total cholesterol levels were statistically significantly
higher than pretest values in baboons fed the unsupplemented
"Western" diet, and that konjac flour supplementation of the
"Western" diet prevented this increase. Although serum levels of
high-density lipoprotein increased with all "Western" diets, the
percentage of total cholesterol as high-density lipoprotein was
statistically significantly greater in baboons fed the konjac flour-
supplemented diet for 9 weeks compared to other diets. Konjac
flour-supplementation also was reported to statistically
significantly increase levels of serum triglycerides and circulating
free fatty acids after 9 weeks. Finally, liver cholesterol
concentration was approximately 30% lower and the area under the
glucose tolerance curve was smaller when baboons were fed konjac
flour-supplemented diets for 9 weeks. Because similar effects were
seen with the sodium propionate-supplemented diet, the effects
observed in baboons fed konjac flour-supplemented "Western" diets
may be due to colonic production and absorption of propionate from
this soluble fiber (Venter et al., 1990).
2.2.10 Special studies on nutrient absorption
Kiriyama and coworkers (1974) studied the effects of chemically
pure, water-soluble konjac flour (test article was "purified by the
method of Sugiyama" and purity was tested) on transport of bile
acids in everted ileal sacs of rats. Small intestines (not
including the duodenum) from adult male and female Wistar rats were
excised, cut into segments, everted, and tied into sacs; these sacs
were used to evaluate the uptake of 14C-labelled cholate or
taurocholate in vitro. Results of this experiment confirmed that
the rat ileum actively transports cholic acid against a
concentration gradient. Active transport of cholic or taurocholic
acid was significantly inhibited (2-3-fold) when 0.25% konjac flour
was added to the media outside of sacs made from the ileum (distal
small intestine) but not when 0.25% konjac flour was added to the
media outside of sacs made from the jejunum (proximal small
intestine). However, there was no inhibition of transport in the
presence of 0.05% konjac flour. No inhibition of transport was seen
when everted ileal sacs were incubated in a konjac flour-free bile
acid medium after the sacs had been pre-immersed in 0.25% konjac
flour. This suggests that the binding of konjac flour to the
surface of the intestinal mucosa is not strong enough to effectively
inhibit the active transport of bile acids. This report suggests
that konjac flour does not bind, sequester, or adsorb bile acids
since, in a simple dialysis experiment, the equilibrium of bile
acids across a cellophane membrane was not altered by the presence
of konjac flour on one side of the membrane (Kiriyama et al.,
1974).
Because previous studies (Reinhold et al., 1975 and 1976)
have shown that plant fibers bind minerals, including calcium, zinc,
and iron, thereby rendering them unavailable for intestinal
absorption, Oku et al. (1982) studied the influence of dietary
konjac flour and other nutritionally unavailable carbohydrates on
intestinal absorption of calcium. Six male Wistar rats/group
(initial body weight, 40-50 g) were fed ad libitum a basal diet
containing 67% corn starch (control) or the same diet in which 20%
cellulose I, 20% cellulose II, 10% konjac flour, 20% konjac flour,
or 20% pullulan had been substituted for an equal amount of corn
starch (konjac flour was identified as having been derived from
Amorphophallus konjac). Rats were fed control or experimental
diets for 7 or 8 weeks. Each rat was placed in a metabolic cage for
three days at the end of the study. Body weights were recorded
weekly; feed consumption was determined daily during the last 3 days
of the study.
Compared to rats fed the control diet, rats fed diets
containing 10% and 20% konjac flour had significantly reduced mean
body weights (control: 328 g; 10% konjac flour: 296 g; 20% konjac
flour: 258 g). Feed consumption of rats fed diets containing 10% or
20% konjac flour, however, was approximately the same as feed
consumption of control rats. Serum levels of calcium and inorganic
phosphorus were not statistically significantly altered in animals
fed diets containing konjac flour, although serum calcium levels
showed a declining trend. In in vitro investigation of calcium
transport using everted duodenal sacs from treated and control rats,
calcium transport was significantly reduced (to 60% of control
value) in the 20% konjac flour-fed group only. Calcium binding
activity in the supernatant of homogenized duodenal mucosa was also
significantly depressed in all groups of rats fed diets containing
20% carbohydrate diets, with the greatest effect associated with
consumption of diets containing 20% konjac flour (50% of control
binding). Based on these results, consumption of unavailable
carbohydrates, including konjac flour, may be associated with
decreased function of intestinal epithelial protein(s) essential for
transport of calcium. As well, because consumption of konjac flour
appeared to be associated with a functionally compromised
gastrointestinal mucosal surface, absorption of minerals other than
calcium may also be affected (Oku et al., 1982).
2.3 Observations in humans
Several experiments were performed to evaluate the effects of
konjac fiber on glucose metabolism in normal and diabetic subjects.
After a 12-hour fast, 3.9 g konjac flour (test substances were
identified as "powdered glucomannan", viscosities were 100-150 000
cP [konjac flour], 52 000 cP [low-viscosity konjac flour], or
194 800 cP [high-viscosity konjac flour]) was consumed either
simultaneously with or 15 min. before a glucose load or test meal
(This dose was selected because of reports that Japanese subjects
experienced abdominal pain and complications following consumption
of 5.2 g or more konjac flour.) Venous blood samples were drawn at
0 (fasting), 30, 60, 90, 120, and 180 min. after glucose or test
meal consumption. When meals containing konjac flour were fed to
seven non-diabetic subjects, mean serum glucose was significantly
below levels for control, non-diabetic subjects at 30, 60, 120, and
180 min. Serum insulin levels were also significantly decreased at
30, 60, and 90 min. in these subjects. Less pronounced effects were
observed when konjac flour was administered 15 min. before meals;
under these circumstances, serum glucose levels were significantly
reduced at 30 and 180 min. only. In a similar experiment involving
six non-insulin-dependent diabetics, significant reductions in mean
serum glucose levels were observed at 30 and 60 min. following
consumption of konjac flour. However, no significant reductions in
serum glucose levels were observed when guar gum, another
gel-forming fiber consisting of galactose and mannose in a molar
ratio of 1:2, was fed to subjects instead of konjac flour.
In a study with nine subjects, low-viscosity konjac flour
delayed the increase in serum glucose from 30 min. (seen in subjects
fed a meal without konjac flour) to 60 min (when the same subjects
were fed an identical meal containing konjac flour). In addition, a
high-viscosity konjac flour was more effective in delaying the rise
in serum glucose following consumption of a konjac flour-containing
meal than the low viscosity konjac flour.
Absorption of xylose was measured following administration of
25 g xylose and 50 g glucose to each of five healthy volunteers.
Co-administration of 3.9 g konjac flour caused a significant
decrease in the excretion of xylose after two hours and appeared to
prolong the time required for absorption of xylose, since total
xylose excretion after 6 hours was similar in konjac flour-fed and
control subjects (no data presented).
When each of 21 diabetic subjects was fed 7.2 g konjac flour
daily for 17 days, mean fasting serum glucose levels were
significantly decreased throughout the study. When observed for 90
days after daily feeding of 7.2 g konjac flour for 17 days (no data
presented), mean serum cholesterol levels decreased significantly
for the first 38 days, then gradually increased; triglyceride and
HDL-cholesterol levels, however, were reported not to have been
affected (Doi et al., 1982).
Following an overnight fast, seven young men (22-32 years old;
110±6% of ideal Japanese body weight) were given a 500 ml solution
containing 80 g glucose (controls) or a similar solution containing
80 g glucose and 5 g konjac flour (konjac flour was identified as
having been prepared fresh from Amorphophallus konjac after prompt
inactivation of tuber mannanase I and mannanase II by homogenization
with ethanol). One week later, the same experiment was performed,
but treatments for each group of subjects were reversed. Plasma
glucose and insulin levels were measured in venous blood samples
collected from each subject at 0 (fasting sample), 30, 60, 90, 120,
and 180 min after consuming control and konjac flour-containing
glucose solutions. In control and konjac flour-fed subjects, plasma
glucose and insulin levels peaked within 30 min.; however, both
parameters were lower (the decrease in serum insulin was
statistically significant) when subjects consumed the glucose
solution containing konjac flour. At 60, 90, and 120 min. following
administration of the konjac flour-containing glucose solution,
serum glucose and insulin levels were decreased compared to samples
following administration of the control glucose solution, although
the decreases were not statistically significant; at 180 min.,
however, serum glucose and insulin levels were increased in subjects
administered the konjac flour-containing glucose solution. Thus,
when subjects were challenged with glucose, plasma glucose and
insulin levels returned more slowly to fasting levels when konjac
flour was co-administered with the glucose. Despite the time course
differences in plasma glucose in subjects following administration
of a glucose solution or a konjac flour-containing glucose solution,
the total areas under the plasma glucose curves for 0-180 min. were
identical. However, the total area under the plasma insulin curve
was significantly smaller after administration of the konjac flour-
containing glucose solution than after administration of the control
glucose solution. These results suggest that soluble dietary fibers
such as konjac flour have beneficial effects on serum glucose levels
and that these effects may be due to delayed stomach emptying and
delayed glucose diffusion in the intestinal lumen (Ebihara et al.,
1981).
The effects of konjac flour on serum glucose levels were
evaluated in 72 type II diabetic subjects (mean age 55, range 39-76)
by Huang and coworkers; subjects were grouped as mild, moderate, or
severe diabetics. Meals containing 2% refined konjac flour in the
form of konjac toast or konjac noodles were consumed by test
subjects (average intake was 8.6 g konjac flour/day) for
approximately 65 days. Weekly food intakes were recorded three
times: before konjac flour-ingestion began and during weeks three
and seven of the study. Fasting venous blood samples and 2-hr
postprandial blood samples (before and after breakfast,
respectively) were drawn once before konjac flour-ingestion began
and on days 30 and 65 of the study; the following determinations
were made: fasting blood glucose (FBG), 2-hour post-prandial blood
glucose (PBG), glycosylated haemoglobin (GHB), total cholesterol
(TC), high-density lipoprotein cholesterol (HDL-C), low-density
lipoprotein cholesterol (LDL-C), and triglyceride (TG). Compared to
levels measured before konjac flour-ingestion began, there were
statistically significant reductions in FBG levels on days 30 and 65
and in GHB on day 65. Konjac flour appeared to be particularly
beneficial to subjects with higher levels of blood glucose because
the extent of konjac flour-associated decreases in FBG and PBG
appeared to be directly proportional to the severity of subjects'
pre-test levels of FBG and PBG. For instance, mild, moderate, and
severe diabetic groups had the following initial vs. final FBG
levels: 129.4±10.5 vs. 124.0±26.8; 165.9±10.9 vs. 142.6±35.3; and
227.0±25.3 vs. 171.4±37.4, respectively. Finally, the study
reported a positive correlation between konjac flour-associated
decreases in FBG and PBG.
In general, food containing konjac flour did not appear to have
a significant effect on blood lipids. Several subjects were
reported to have experienced weight loss during the study: the mean
weight loss of 42/59 subjects at 30 days was 1.8 kg (range
0.2-4.7 kg) and the mean weight loss for 41/51 subjects at 65 days
was 2.2 kg (range 0.5-6.0 kg).
In this study, subjects reported the following symptoms
associated with consumption of meals containing konjac flour: 69-90%
of the subjects reported improved appetite, polyuria at night,
thirst, and constipation or soft stool; on the other hand, 40
subjects reported a total of 45 symptoms, such as loose stool,
flatulence, diarrhoea, and abdominal pain, sounds, or distension
(Huang et al., 1990).
A recent study compared the effects of four non-starch
polysaccharides, including konjac flour, on glucose tolerance,
insulin secretion, gastric emptying, and gut hormone secretion in 12
healthy male volunteers (mean age = 19.5 years). Subjects were
divided into two groups; on three separate occasions (at least one
week apart) and following an overnight fast, members of each group
were given a test meal (white bread, honey, and orange squash
containing 100 g carbohydrate) either with or without 10 g soya-bean
cotyledon fiber (SCF) or 5 g konjac flour. Soluble paracetamol
(1.5 g dissolved in 150 ml water) was consumed simultaneously with
each meal; over the following 180 min., plasma levels of paracetamol
were measured as an index of liquid gastric emptying. Plasma
concentrations of glucose, insulin, and gastric inhibitory
polypeptide (GIP) were measured during the same time period. Konjac
flour-supplemented meals had a significant depressive effect on
post-prandial insulin levels, where peaks for control and konjac
flour-supplemented meals were 96.2±11 and 64.3±2.6 mU/l,
respectively. The 0-90 min. incremental area under the insulin
curve was significantly reduced following consumption of a konjac
flour-supplemented meal (82% of area following consumption of a
control meal), although consumption of a meal containing SCF
increased this parameter (119% of area following consumption of a
control meal). Post-prandial plasma glucose, GIP and paracetamol
levels were not affected by consumption of meals containing konjac
flour or SCF (Morgan et al., 1990).
Results of this study are consistent with results reported in
similar experiments by Ebihara et al. (1981) but were inconsistent
with results reported by Doi et al. (1982), which Morgan and
coworkers attributed to possible differences in the composition of
test meals (not specified in the study by Doi et al., 1982) that
may have affected gastric emptying.
Zhang and coworkers studied the effects of consuming konjac
flour-supplemented diets (5 g konjac flour/day) for 45 days on human
lipid metabolism in elderly subjects with hyperlipidaemia. Subjects
were described as having borderline risk levels of serum
triglycerides (200-230 mg/dl), hypercholesterolaemia (>230 mg/dl),
borderline risk levels of serum triglycerides (130-150 mg/dl),
hypertriglyceridaemia (>150 mg/dl), or both hypercholesterolaemia
and hypertriglyceridaemia. Subjects were randomly divided into two
groups: the konjac flour group (66 subjects) consumed normal
Japanese diets supplemented with foods containing konjac flour
(3 g/day for the first 2 or 3 days, then 5 g/dy for the rest of the
study); the control group (44 subjects) consumed normal Japanese
diets without konjac flour supplementation; a recovery group (46 of
66 subjects in the konjac flour group) consumed normal Japanese
diets for an additional 45 days. Venous blood samples were drawn
before breakfast before the study began, at the end of the study
(45 days) and at the end of the recovery period (an additional 45
days). Konjac flour used in this study was described as "konjac
meal...in the form of noodles, breads, cakes, etc., to which it was
added, or after it was cooked directly with milk, soya-milk, soup,
water, or stuffing."
After consumption of konjac flour for 45 days, subjects had
statistically significantly decreased levels of serum total
cholesterol, triglycerides, and low-density lipoprotein and
statistically significantly increased levels of high-density
lipoprotein and apoprotein; however, changes in these parameters in
the control group during the study were not significant. In
addition, konjac flour subjects had statistically significantly
decreased body weight, serum total cholesterol, serum triglycerides,
and serum low-density lipoprotein and increased serum high-density
lipoprotein compared to control subjects after 45 days. After
consumption of konjac foods, 27 subjects had statistically
significant decreases in body weight (0.5 to 4.7 kg at 45 days);
subjects consuming konjac flour reported decreases in dizziness and
headaches (9/66) and chronic constipation (13/66); however, subjects
also reported that they excreted more bulk faeces (17/66),
experienced diarrhoea (3/66), and had increased hunger (4/66).
After the 45-day recovery period, subjects (46 of 66 subjects who
had previously consumed konjac flour for 45 days) had statistically
significant increases in serum total cholesterol and low-density
lipoprotein and a statistically significant decrease in high-density
lipoprotein; serum triglyceride levels remained the same. This
report concluded that beneficial effects observed in
hypercholesterolaemic patients following consumption of 5 g konjac
flour/day for 45 days were reversible upon discontinuance of konjac
flour in the diet (Zhang et al., 1990).
The efficacy of konjac flour (test substance identified as
"glucamannan") for weight loss in overweight osteoarthritic patients
was evaluated in a double-blind crossover study. Twenty outpatients
(3 men and 17 women; mean age 53 years, range 30-68 years) were
divided into two groups. For the first two months of the study,
each subject was administered 1.5 g of konjac flour or a placebo
before breakfast and dinner; for the following two months,
treatments were reversed. Sixteen subjects completed the study; one
subject stopped because of abdominal discomfort during the konjac
flour-treatment period. Body weight was recorded monthly.
Decreases in body weight during konjac flour-phases of the study
(first group of subjects: mean body weight decreased from 73.7 to
70.1 kg; second group of subjects: mean body weight decreased from
79.0 to 76.4 kg) were reported to be statistically significant and
were attributed to konjac flour administration. Study stated that
subjects experienced no changes in blood pressure, heart rate, or
clinical chemistry, but no data were provided (Biancardi et al.,
1989).
The effect of konjac flour on weight loss and blood levels of
total cholesterol, total triglycerides, and low-density lipoprotein
was investigated in a double-blind study of obese women for 8 weeks.
Twenty obese women (weights were at least 20% over ideal body
weights) were randomly assigned to two groups (10/group) so that
weight and height distributions for each group were similar. The
konjac flour group took two capsules of a supplement containing
500 mg "purified glucomannan" three times a day (with 8 oz water),
one hour before each meal, for 8 weeks; control subjects took a
similar capsule containing 500 mg starch under the same conditions.
At the beginning of the study and at 4 and 8 weeks, subjects were
weighed and blood samples were drawn. There were statistically
significant decreases in weight, serum cholesterol and serum
low-density lipoproteins in the konjac flour group compared to the
control group at weeks 4 and 8. A statistically significant
decrease in serum triglycerides occurred at four weeks, but the
decrease was not statistically significant at 8 weeks. This study
suggests that konjac flour can be used for weight reduction and
serum cholesterol reduction in obese patients (Walsh et al.,
1984).
The efficacy of konjac flour was studied in 93 patients with
chronic constipation; 78 patients completed the study. In this
non-controlled, open study, patients were treated with 1 g konjac
flour/day for one month, followed by 1 g konjac flour every other
day for one month. Statistically significant improvements were seen
in several measures of bowel function (number of days per week with
bowel movements and number of enemas given) that lasted until the
end of the second month. Konjac flour was well accepted by patients
and without significant side effects; in addition, konjac flour
reduced (by approximately 50%) the number of patients reporting
abdominal disturbances by the end of the study (Passaretti et al.,
1991).
The influence of dietary konjac flour (test substance
identified as konjac mannan) on absorption of vitamins E (tocopherol
acetate) and B12 (mecobalamin) was evaluated in six normal
volunteers (aged 20-61) and five maturity-onset diabetic patients
(aged 57-81) by Doi and coworkers. Control meals containing
vitamins E and B12 (500 mg and 3 000 µg, respectively) were
consumed by each subject; test meals to which 3.9 g konjac flour had
been added were consumed by subjects on an alternate day. Vitamin
levels in serum were determined immediately before and 1, 3, 5, 8,
12, and 24 hr after consumption of both meals. In normal subjects,
the peak serum level of vitamin B12 was shifted from 3 hr to 12 hr
when the meal was supplemented with konjac flour; however, no shift
was seen in the 5-8 hr peak time observed in diabetics when konjac
flour was added to the meal. Total absorption of vitamin B12
during 24 hr did not appear to be changed by addition of konjac
flour to the test meal. Intestinal absorption of vitamin B12 was
not disturbed by konjac flour.
Addition of konjac flour to the test meal appeared to
significantly lower serum levels of vitamin E, especially in normal
subjects (by 16-30% at most time points). The results suggested
that viscous forms of dietary fibers, such as konjac flour, may form
a barrier around some (fat-insoluble) substances (including glucose,
essential electrolytes and cations, and possibly vitamin B12),
thereby delaying their absorption rather than causing malabsorption.
On the other hand, because konjac flour consumption may interfere
with the absorption of bile acids, the absorption of the fat-soluble
vitamin E, a process which is dependent on the presence of
conjugated bile acids, may also be impaired by konjac flour
consumption (Doi et al., 1983).
The effect of konjac flour (identified as glucomannan in the
form of konjac flour) on intestinal absorption of glibenclamide, a
sulfonylurea-type hypoglycaemic drug, was evaluated in nine healthy
male volunteers, aged from 21 to 47 years. All subjects
participated, on two consecutive days, in both the control and test
phases of the experiment. Plasma concentrations of the drug were
followed for six hours after subjects received the drug (2.5 g)
alone (control phase) or with 3.9 g konjac flour (test phase); in
both phases, subjects ate breakfast immediately after receiving the
drug. Compared to plasma drug levels during the control phase,
subjects in the test phase had lower drug levels at 30 min. and this
tendency continued for most subjects until at least 180 minutes. In
the control phase, mean plasma levels of glibenclamide peaked
rapidly at 60 min. and declined more slowly; when konjac flour was
administered with the drug, however, there was no apparent peak in
serum drug level. Co-administration of konjac flour with
glibenclamide appeared to increase inter-individual variation in
plasma drug levels. This study also demonstrates that dietary
intake of konjac flour can influence the pharmacokinetics of
co-administered oral drugs (Shima et al., 1983).
When dry, non-expanded konjac flour was marketed as a dieting
aid, 7 case reports of oesophageal obstruction caused by swelling of
these tablets were made. The case reports were reviewed in 1986:
all patients were women taking the konjac flour tablets for weight
loss; obstruction was complete in 5/7 cases and was caused by a
single tablet in all but one case; obstruction was presumably caused
by swelling of dry konjac when hydrated by body fluids; none of the
patients died. Expansion rates of 5 tablets (500 mg konjac flour
each) immersed in water varied, but tablets increased their mean
volumes from one to approximately 16 ml in 10 min; final volumes
ranged from 12 to 17.5 ml. It is important to note that konjac
flour in food is not in this dry form and there are no reported
cases of oesophageal obstruction caused by hydrated konjac gels,
such as those traditionally eaten in Japan (Henry et al., 1986).
Inhalation of konjac dust ("dancing powder" in factories
producing konnyaku, a popular food in Japan made from konjac tubers)
in the workplace has been reported to produce allergic bronchial
asthma (known as konnyaku asthma) in sensitized individuals
(Nakazawa, 1983). In Japan, konnyaku asthma occurs in workers
exposed to konjac dust and in people who live close to konjac
processing facilities. An epidemiological study of Japanese plant
employees and nearby residents conducted in 1980 found that 0.1% of
the population (15 675 people) had konnyaku asthma. Konnyaku asthma
can be treated by desensitization therapy and disappears when the
individual is no longer exposed to konjac dust. It should be noted
that inhalation of konjac powder has also been reported to cause
allergic asthma in sensitized guinea pigs (Banno, 1979), although
application of mechanically ground konjac to the skin of guinea pigs
did not produce skin sensitization reactions (Kotkoskie, 1992). In
both humans and animals, konjac powder or dust has been shown to
produce allergic bronchial asthma by a type I or anaphylactic immune
reaction (Nakazawa, 1983).
3. COMMENTS
The Committee reviewed data from acute and short-term toxicity
studies, as well as studies on embryotoxicity, genotoxicity,
nutrient absorption, anti-carcinogenicity, gastrointestinal effects,
and observations in humans. However, the Committee was concerned
about the lack of information on the fate of konjac flour in the gut
and the inadequacy of the short-term toxicity studies. The
Committee was informed of the existence of a 13-week toxicity study
in dogs and a 4-week toxicity study in rats that were not made
available for review at the present meeting.
Human studies were conducted for up to 65 days at dose levels
of up to 8.6 g konjac flour/person/day. Volunteers consuming
approximately 5.2 g or more konjac flour/person/day reported
symptoms such as loose stools, flatulence, diarrhoea and abdominal
pain or distension. Studies with normal and diabetic volunteers
demonstrated that consumption of 7.2-8.6 g konjac flour/person/day
for 17 days significantly decreased mean fasting serum glucose
levels; in addition, a dose of 3.9-5.0 g konjac flour/person
consumed with a single meal (or administered with glucose) was
reported to delay the increase in serum glucose and insulin levels
for several hours following the meal, thereby also delaying their
return to baseline levels. Consumption of test meals containing
3.9 g konjac flour appeared to impair vitamin E absorption (up to
30% decrease in peak serum levels) and influenced the
pharmacokinetics of the co-administered drug glibenclamide. On the
other hand, intestinal absorption of vitamin B12 or the drug
paracetamol were not affected by consumption of meals containing
konjac flour (3.9 g konjac flour/person for vitamin B12 and 5 g
konjac flour/person for paracetamol).
4. EVALUATION
On the basis of the available toxicological data, particularly
data from human studies, the long history of use of konjac as a food
in China and Japan, and estimates of konjac flour consumption from
traditional and anticipated food additive uses, the Committee
allocated a temporary ADI "not specified" for konjac flour. The
results of additional short-term toxicity studies, which the
Committee was informed have been conducted in rats and dogs,
together with adequate data on the fate of konjac flour in the gut
are required for review in 1996. In view of the observed impairment
of absorption of vitamin E, information on the influence of konjac
flour on the bioavailability of fat soluble vitamins is also
required for review by 1996. The Committee noted that consumption
of dry konjac flour has been associated with oesophageal
obstruction, and recommended that konjac flour be consumed only in
the hydrated form.
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See Also:
Toxicological Abbreviations
Konjac flour (WHO Food Additives Series 37)
KONJAC FLOUR (JECFA Evaluation)