DEXTRINS
Explanation
This substance was evaluated previously for an ADI for man by the
Joint FAO/WHO Expert Committee on Food Additives in 1969 and 1974 (see
Annex I, Refs. 19 and 29). Toxicological monographs were published in
1969 and 1974 (see Annex I, Refs. 20 and 30).
Since the previous evaluation, additional data have become
available and are summarized and discussed in the following monograph.
The previously published monograph has been expanded and is reproduced
in its entirety below.
Introduction
White dextrins are prepared by heating dry starch in the presence
of an acid at a temperature generally below 150°C. White dextrins may
also be obtained by further continuing the acid process for making
thin boiling starches. Because of the nature of the application as
well as their flavour, their use in food is restricted. Dextrins are a
stage in the normal digestion of starch occurring in the human
gastrointestinal tract. They represent a broad range of products with
considerably smaller molecular size than native starch.
Yellow dextrins are prepared in a similar manner but at a higher
temperature and using less acid. Apart from depolymerization, a good
deal of internal rearrangement occurs with formation of highly
branched molecules. These materials are used in foods in limited
quantities as adjuvants in flavour encapsulation and similar minor
uses.
BIOLOGICAL DATA
BIOCHEMICAL ASPECTS
Absorption and metabolism
Dextrins and their parent starches were fed to groups of 6
weanling male rats (strain unspecified), initial weight 45-60 g, at a
level of 60 g/kg bw for 21 to 28 days. Diets contained 18.8% casein.
The digestibility of wheat dextrin was somewhat lower than that of
wheat starch. The potato dextrin gave a higher body weight gain and
digestibility coefficient than the parent starch (Booher et al.,
1951).
In a study on the effect of type of dietary carbohydrate on
B-vitamin synthesis in the digestive tracts of rats, groups of 17 to
44 male and female rats (strain unspecified), 21 days of age were
placed on test diets containing 18% protein (casein), 71%
carbohydrate, and 3% butterfat, cod-liver oil and salt mixture. The
carbohydrate sources used included cornstarch, corn dextrin, glucose,
lactose and sucrose. Animals on all diets, without supplemental
B-vitamins but with access to their faeces, showed low or declining
growth rates after 2 weeks except for the group fed the dextrin diet.
Growth rates in all groups were increased after receiving faeces of
the dextrin-fed group. Rats receiving the dextrin diet had enlarged
caeca at the conclusion of the study. Caecectomized rats with access
to their faeces lost weight when fed a dextrin diet; supplementation
with baker's yeast resulted in weight gain. It was concluded that the
peculiar property of corn dextrin was not due to retained B-vitamins,
but rather to the formation of these vitamins in the lower part of the
digestive tract of the rat as a result of incomplete digestion of this
particular carbohydrate (Guerrant et al., 1935).
Fournier (1959) studied the effect of various dietary
carbohydrate sources on calcium retention, serum calcium levels,
and caecal size in the rat. Wistar rats (sex unspecified) weighing
62-74 g, were fed a low calcium diet (50 mg Ca/100 g diet) for 18 days
after which groups of 6 rats were placed on diets containing 15%
casein, 1.5% calcium carbonate and 45-70% experimental carbohydrate
(starch, dextrin, caramel or glucose) plus cereal grain to bring total
carbohydrate to about 70%. Rats received an estimate of 46 g dextrin
per kg body weight. Calcium balance was determined during the third to
fifth day; after 10 days the rats were sacrificed and serum calcium
determined. Caecal enlargement observations were made after 2 weeks of
feeding a diet containing 75% of the experimental carbohydrate
source, 12% casein, 8% peanut oil and 3% salts. Calcium intake was
approximately the same for all diets, but calcium retention for the
dextrin and caramel diets was nearly double that for the starch and
glucose diets. Serum calcium levels also were greater for the dextrin
and caramel diets. Dry caecal weights of rats fed dextrin and caramel
were more than double those fed the starch and glucose diets. The
author postulated that dextrin and caramel were less easily
metabolized than their parent substances, starch and glucose, and that
this property contributed to the effects observed.
14C-labelled beta-cyclodextrin homogenized in aqueous dextran
was administered to 5 Wistar plus Long Evans F1 hybrid male rats
weighing about 200 g each. Individual animals received doses
corresponding to their body weight through an oesophageal cannula.
Three control animals received 14C-labelled glucose. Blood levels of
the compounds were measured at intervals up to 97 hours from tail vein
samples. At 7, 12 and 24 hours after administration, selected animals
were decapitated, and radioactivity was measured in stomach, small
intestine and colon. In the case of the cyclodextrin, a maximum of
only 5% of the administered activity could be found in blood even
after 10 hours; after 96 hours the same residual radioactivity was
found in the blood with both glucose and ß-cyclodextrin. This study
suggests that ß-cyclodextrin cannot be absorbed either from the
stomach or the small intestine; only the labelled open-chain dextrins
and glucose formed from cyclodextrin by amylase action were absorbed
(Szejtli et al., 1980).
TOXICOLOGICAL STUDIES
Special studies on nephrosis in the rat kidney due to alpha- and
beta-cyclodextrin
Groups of 5 male and 5 female Sprague-Dawley rats weighing 150 to
160 g were administered cyclodextrins intravenously. The i.v. LD50
for rats was determined to be 0.79-1.0 g/kg bw with a close
relationship between the acute toxicity and the nephrotoxic dose
(Frank et al., 1976).
Groups of 4 100-124 g Sprague-Dawley rats received single s.c.
doses of cyclodextrins of 0.225, 0.45 or 0.90 g/kg and were killed 12,
24, 48 or 96 hours later. Controls received saline injections. Kidneys
were sectioned for light microscopy and histopathological observations
(Frank et al., 1976).
In another experiment, groups of 4 100-125 g Sprague-Dawley rats
were given 1, 2, 3, 4 or 7 daily s.c. injections of cyclodextrins at
0.225, 0.45, 0.675, 0.90, 0.1 or 1.0 g/kg bw. Controls received saline
injections. Rats were killed 24 hours after the last injection and
kidneys were sectioned for histopathological observations (Frank et
al., 1976).
Renal toxicity due to the cyclodextrins was shown to result from
a series of alterations in the vacuolar organelles of the proximal
convoluted tubules. Intracellular concentration of toxin via the
lysosomal pathway resulted in a change of the physiological function
of the proximal tubule which ultimately leads to cell death (Frank et
al., 1976).
Short-term studies
Rat
Groups of 10 male Wistar rats received diets with 6 or 15%
protein from casein and 77 or 66% carbohydrate (75 and 65 g
carbohydrate/kg bw). After 28 days, protein efficiency and weight
gain/g of dry food were significantly lower for corn dextrin than for
cornstarch, but were greater or equal to values for dextrose. Corn
dextrin diets caused no unusual effect on liver weight or liver fat
content; however, rats receiving corn dextrin exhibited a slight
diarrhoea and caecal enlargement to about twice that in rats fed
unmodified cornstarch (Reussner et al., (1963).
Groups of 6 Sprague-Dawley male weanling rats (initial weight
40-50 g), were fed for periods of 2-12 weeks on diets containing
approximately 80 g dextrin/kg bw; diets contained 81% carbohydrate, 9%
casein and 5% corn oil. Rates of gain with the dextrins over a 4-week
period were about 15% less than that for autoclaved cornstarch; the
latter weight was about double when the carbohydrate source was
glucose or sucrose. Liver fat deposition was less for one of the
dextrins, cornstarch or glucose, than for sucrose as the carbohydrate
source. Liver fat deposition values were not reported for the other
dextrin (Harper et al., 1953).
Groups of 5 or 10 male weanling Sprague-Dawley or Osborne-Mendel
rats, weighing initially 40-50 g, were fed diets containing about 80 g
carbohydrate/kg bw; diets consisted of 87% carbohydrate, 9% casein, 3%
gelatin and 3% corn oil. Weight gain over a 4-week period with niacin
supplementation was the same with either dextrin, starch or glucose as
carbohydrate source, without niacin supplementation, growth rate
decreased about 40% for starch and dextrin as the carbohydrate source,
as compared to 60% decrease with glucose as the carbohydrate source,
suggesting a lesser niacin requirement with starch and dextrin as
carbohydrate source (Hundley, 1949).
Long-term studies
Groups of 9 male Sprague-Dawley rats (2 months of age) were fed
diets with different sources of carbohydrate for a 20-month period.
Diets consisted of rat chow mixed with 20%, by weight, of the various
carbohydrate sources, including dextrin, sucrose, and dextrose. Rats
received approximately 10 g experimental carbohydrate/kg bw. Protein
efficiency ratios calculated after 6 months feeding were nearly equal
for the dextrin, dextrose and sucrose diets and significantly higher
than for the basal rat chow diet. Weight gain after 20 months of
feeding was about 5% less for dextrin than for dextrose or sucrose but
about 5% more than on the basal rat chow (Cohen et al., 1967).
Comments
These substances are regarded as identical to the intermediates
formed in the normal digestion of starch and normal constituents of
food.
EVALUATION
Estimate of acceptable daily intake for man
Not specified.*
* The statement "ADI not specified" means that, on the basis of the
available data (toxicological, biochemical, and other), the total
daily intake of the substance, arising from its use or uses at
the levels necessary to achieve the desired effect and from its
acceptable background in food, does not, in the opinion of the
Committee, represent a hazard to health. For this reason, and for
the reasons stated in individual evaluations, the establishment
of an acceptable daily intake (ADI) in mg/kg bw is not deemed
necessary.
REFERENCES
Booher, L. E., Behan, I. & McMeans, E. (1951) Biological utilization
of unmodified and modified food starches, J. Nutr., 45, 75-95
Cohen, L., Perkin, E. G. & Dobrilovic, L. (1967) The manifold effects
of different dietary carbohydrates, Progr. Biochem. Pharmacol.,
2, 182-202
Fournier, P. (1959) Le caramel et la dextrine préparés par action de
la chaleur sèche sur le glucose et l'amidon possèdent les
qualités physiologiques des composés de structure, C. R. Acad.
Sci., 248, 3744-3746
Frank, D. W., Gray, J. E. & Weaver, R. N. (1976) Cyclodextrin
nephrosis in the rat, Am. J. Pathol., 83(2), 367-382
Guerrant, N. B., Dutcher, R. A. & Tomey, L. F. (1935) The effect of
the type of carbohydrate on the synthesis of B vitamins in the
digestive tract of the rat, J. Biol. Chem., 110, 223-243
Harper, A. E. et al. (1953) Influence of various carbohydrates on the
utilization of low protein rations by the white rat, J. Nutr.,
51, 523-537
Hundley, J. M. (1949) Influence of fructose and other carbohydrates on
the niacin requirement of the rat, J. Biol. Chem., 181, 1-9
Reussner, G., Jr, Andros, J. & Thiessen, R., Jr (1963) Studies on the
utilization of various starches and sugars in the rat,
J. Nutr., 80, 291-298
Szejtli, J., Gerl'oczy, A. & F'Onagy, A. (1980) Intestinal absorption
of the 14C-labelled beta-cyclodextrin in rats, Arzneim.,
30(5), 808-810
See Also:
Toxicological Abbreviations