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Department of Biological Resources, Faculty of Agriculture, Ehime University, 3-5-7 Tarumi, Matsuyama 790, Japan
1To whom correspondence should be addressed. E-mail: ebihara{at}agr.ehime-u.ac.jp
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • tapioca starch • hydroxypropyl distarch • phosphate • physiological effect • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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2
3
4
5
,51
,52)
.
Therefore, CMS would be expected to exert physiological effects similar
to those of dietary fiber. The presence of CMS in the gut digesta may
influence the digestion of other nutrients and absorption of other
compounds. CMS may influence cholesterol and bile acid metabolism and
the absorption of minerals as a result of fermentation. It has been
reported that the large intestine may represent a major site of Ca and
Mg absorption when acidic fermentations take place (6)
.
Therefore, CMS would be expected to exert physiological effects similar
to those of dietary fiber. The physiological effects of dietary fibers are due to their physico-chemical properties. The enzymatic susceptibility of a CMS is affected by the type of modification, such as substitution or cross-linking. However, there are only a few reports on whether different types of CMS have different physiological effects. Hydroxypropyl distarch phosphate (HDP), a starch that can be modified by a combination of substitution and cross-linking, is one of the CMS used extensively in the food industry. Therefore, we evaluated the physiological effects of six different types of HDP from tapioca starch that have two different degrees of substitution and three different degrees of cross-linking.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The following six kinds of gelatinized HDP with two degrees of
substitution (LS or HS) and three degrees of cross-linking (LC, MC
or HC) were used: LS-LC, LS-MC, LS-HC, HS-LC, HS-MC and
HS-HC (Table 1
). The hydroxypropyl substituents were introduced by causing the tapioca
starch to react with propylene oxide at pH 9–10 in the presence of
Na2SO4. Cross-linking
of the etherified starch was performed with
Na3(PO3)3
(0.02, 0.12 or 0.5 g/100 g etherified starch) at pH 9–10. All
derivatives, as well as the unmodified tapioca starch, were delivered
to the rats in a gelatinized form. The DS was measured according to the
method of Johnson (7)
. The DSP of each HDP was measured
using a slight modification of the method described by Leach et al.
(8)
. Briefly, 1 g of a dry HDP sample was accurately
weighed and placed into a 50-mL graduated centrifuge tube. After adding
1 mL of methanol, distilled water that had been kept at 25°C was
added while mixing with a glass rod until the total volume was 50 mL.
The graduated centrifuge tube was occasionally shaken in a water bath
at 25°C over 20 min to prevent the precipitation of HDP. After
centrifugation at 1200 x g at room temperature for 30
min, the volume of the aqueous supernatant was measured. Then, the
total sugar content in the aqueous supernatant was analyzed with
phenol/H2SO4 reagent
(9)
. The weight of the precipitate of swollen granules was
measured. The DSP of each HDP was calculated as follows:
 |
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where A is total sugar content in the supernatant (mg), B is precipitate (mg) and S is solubility (%).
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showed that there is an inverse
relationship between the DC and the DSP of starch granules. Therefore,
the DC of the three HDPs increased in the following order: LC < MC < HC. Measurement of the level of amylase-resistant starch.
Amylase-resistant starch is starch that cannot be hydrolyzed to glucose
by amylolytic enzymes. To determine the level of amylase-resistant
starch in each HDP, 1-g triplicate samples were incubated with
heat-stable 
-amylase (Termamyl 120L; Novo Nordisk, Copenhagen,
Denmark) at pH 6.0 at 100°C for 30 min and then allowed to cool.
After cooling, the pH was adjusted to 4.5 by HCl, and the samples were
incubated with amyloglucosidase (Sigma A-9913; Sigma Chemical, St.
Louis, MO) at 60°C for 30 min. After the incubation, the amount of
glucose in the hydrolysate was enzymatically determined using
pyranoseoxidase (Determiner GL-E; Kyowa Medix, Tokyo, Japan). The
concentration of amylase-resistant starch was calculated as
follows:
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where wt. sample is the initial weight (g), and G is the weight of the hydrolysate (g).
Animals and diets.
This study was approved by the Laboratory Animal Care Committee of Ehime University, and the rats were maintained in accordance with the "Guidelines for the Care and Use of Laboratory Animals" of Ehime University.
Male Wistar rats (Japan SLC, Hamamatsu, Japan) with an initial weight
of 
80 g were used in these experiments. The rats were housed
individually in cages with screen bottoms of stainless steel in a room
maintained at 23 ± 1°C with a 12-h light/dark cycle (light, 0700–1900h). The rats were acclimated by feeding a commercial solid
diet (MF; Oriental Yeast, Osaka, Japan) for 7 d. After
acclimation, the rats were divided into seven groups of six rats each
(each group had a similar mean body weight). The composition of diets
used in the experiment is shown in Table 2
. The rats were given free access to the experimental diet and water for
21 d. The body weight and food intake were recorded daily for each
rat in the morning before the diet was replaced. Then, the condition of
the feces of each rat was observed.
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Before the rats were killed, feces were collected on the final 3 d
of the experimental period from each rat. The feces were
freeze-dried, weighed and milled. The level of nitrogen (N) in the
diet and feces of each rat was analyzed in duplicate for each
collection according to the Kjeldahl method (11)
. The
apparent digestibility of protein (N x 6.25) was calculated by
measuring the N content in the food and feces. To determine the levels
of Ca, Zn, Fe and Mg, the powdered feces (70 mg) and diet (500
mg) were wet-ashed in HNO3/HClO4 (3:1). The
concentrations of Zn, Fe and Mg in the ashed solutions were measured by
atomic absorption spectrophotometry (AA-6400F; Shimadzu, Kyoto, Japan)
after dilution with deionized water. The calcium concentration in the
ashed solutions was measured by atomic absorption spectrophotometry
after dilution with 10 mol lanthanum chloride/L. The apparent
absorption of Zn, Fe, Mg or Ca was calculated as the difference between
the dietary intake and fecal excretion of Zn, Fe, Mg or Ca,
respectively. Fecal steroids were extracted with a mixture of
chloroform/methanol (1:1, v/v) at 70°C for 60 h
(12)
. Total fecal bile acids were determined enzymatically
by the 3-hydroxysteroid dehydrogenase assay method of Sheltaway and
Losowsky (13)
using taurocholic acid as the standard.
Blood was collected from the abdominal aorta of rats under sodium pentobarbital (50 mg/kg body mass, Nembutal; Abbot Laboratories, North Chicago, IL) anesthesia in a blood collection tube (Vacutainer; Becton Dickinson, Franklin Lakes, NJ) that contained heparin as an anticoagulant. The plasma was separated by centrifugation at 1400 x g at 4°C for 15 min and was stored at -50°C until analysis. The liver was removed, weighed and stored at -50°C for further analysis.
After blood collection, the cecum was removed and weighed. The contents
were transferred to a cooled 50-mL vial and homogenized under
CO2 gas. The water content of the cecal content was
determined as the difference between the wet mass and the dry mass of
the cecal content after freeze-drying. The cecal pH was
measured immediately after removal with a compact pH meter using a
sampling sheet (model C-1; Horiba, Tokyo, Japan; calibrated at 20°C).
The cecal wall was flushed with ice-cold saline (9 g NaCl/L,
4°C), blotted onto filter paper and weighed. The level of cecal
ammonia was determined spectrophotometrically in the deproteinized [4
mL of 0.25 mol sulfuric acid and 50 g sodium tungsten dihydrate
per L, 1:1 (v/v), for 50 mg contents] supernatant (1500 x g, 10 min) of the cecal content (14)
.
The levels of cecal organic acids (acetic, propionic,
n-butyric, succinic and lactic acids) were measured
using HPLC (LC-6A; Shimadzu, Kyoto, Japan) by the internal standard
method. Approximately 300 mg of the cecal content was homogenized by
ultrasonication (USC-6; Iwaki Glass Ltd., Chiba, Japan) in 2 mL of 10
mmol sodium hydroxide/L aqueous solution, containing 0.5 g
crotonic acid/L (Nakarai, Kyoto, Japan) as an internal
standard, in an ice-water bath, and then centrifuged at 10,000
x g for 15 min. The fat-soluble substances in
the supernatant were removed by extraction with chloroform.
Neutralization of the cecal content with sodium hydroxide prevented the
extraction of the individual target organic acid or crotonic acid by
chloroform. The aqueous phase was filtered through a membrane filter
(cellulose acetate, pore size 0.45 µm; DISMIC-13cp; Toyo Roshi, Ltd.,
Tokyo, Japan). These samples were subject to HPLC for analysis of the
organic acids. The organic acids were separated with an ion exclusion
column and detected according to the postcolumn pH-buffered
electroconductivity detection method (16)
using an
H-type cation exchanger column (shim-pack SCR-102H, 8 mm i.d. x 30
cm long; Shimadzu, Kyoto, Japan), column temperature 45°C, with a
mobile phase of 2 mmol perchloric acid/L (flow rate: 1 mL/min, 45°C).
They were then reacted with a commercial detection reagent (ST3-R; 15
mmol disodium hydrogen phosphate/L), 5 mmol p-toluene
sulfonic acid/L aqueous solution (flow rate, 0.8 mL/min, 45°C), an
electroconductivity detector of positive polarity at 45°C (CDD-6A;
Shimadzu) and a detection reagent of 20 mmol bis-Tris/L aqueous
solution containing 5 mmol p-toluene sulfonic acid/L and
100 µmol EDTA/L (flow rate 0.8 mL/min, 45°C).
The levels of triglyceride and total cholesterol in the plasma were
enzymatically determined with commercial kits (Triglyceride E-Test
Wako and Cholesterol E Test Wako; Wako Pure Chemical Industries, Osaka,
Japan). The level of liver total lipids was determined gravimetrically
after extraction according to the method of Folch et al.
(15)
. The levels of liver triglyceride and total
cholesterol were also measured. Lipids were extracted from 500 mg liver
with chloroform/methanol (2:1, v/v) according to the method of Folch et
al. (15)
. After extraction, the volume of the lipid
solution was adjusted to 20 mL with the same solution of
chloroform/methanol (2:1, v/v). One mL of this extract was dried under
a nitrogen stream, and the obtained residue was mixed with 100 µL
isopropyl alcohol containing 100 g Triton X-100/L (Wako Pure
Chemical Industries). Thirty µL of this mixture was mixed with 3 mL
of aqueous enzyme solution according to the standard procedure of the
assay kit (Triglyceride E-Test Wako and Cholesterol E-Test
Wako; Wako Pure Chemical Industries), and the triglyceride and
cholesterol concentrations were determined colorimetrically. In a
preliminary study, 30 µL of isopropyl alcohol containing 100 g
Triton X-100/L did not affect the enzymatic reactions (data not shown).
Statistical analysis.
Data are expressed as means ± SEM. The statistical significance of a difference between the control group and each HDP group was evaluated by one-way analysis of variance followed by Student-Newman-Keuls test using the Super ANOVA statistical software package (Abacus Concepts, Berkeley, CA).
The effects of the DS and DC were analyzed by two-way ANOVA, using
a computer software package (StatView Version 4.5; Abacus Concepts),
and the difference among groups was examined using Duncan’s new
multiple range test when the F-value was significant.
Differences were considered to be significant at P
< 0.05. Correlation coefficients were determined by linear
regression (17)
.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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. The level of amylase-resistant starch in the HS
diets was more than twice as much as that in the respective LS diet
with the same DC. The level of amylase-resistant starch slightly
increased with increasing DC.
Loose stools or diarrhea was observed in the rats fed the LS and HS
diets, but intestinal adaptation took place during the 1st wk of
feeding. The severity of diarrhea was not affected by the DS of the
HDP, but increased with increasing DC. Body mass gain, food intake and
feed efficiency were not affected by the type of diet (Table 3
). The weight of the cecal contents and cecal wall of the rats fed the
HS diets was significantly higher than the respective weight in the
control rats and was also significantly higher than the respective
weight in the rats fed the LS diets. The moisture in the cecal contents
of rats fed the LS-MC, LS-HC or HS diets was significantly lower
than that in the control rats, and the moisture in the cecal contents
of rats fed the HS diets was significantly lower than that in the rats
fed the LS diets; however, the level of moisture in the cecal content
was not related to the DC. The wet weight of the fecal output of the
rats fed the LS-HC diet or the HS diets was significantly higher
than that of the control rats. The wet weight of the fecal output of
the rats fed the HS diets was significantly greater than that of the
rats fed the LS diets, and it increased with increasing DC. The
moisture of the fecal output was significantly higher in the rats fed
the LS-HC diet or the HS diets than in the control rats. The
moisture absorbed in the colon was significantly lower in the rats fed
the LS-HC or HS diets than in the control rats, and the moisture
absorbed in the colon of the rats fed the LS and HS diets gradually
decreased with increasing DC.
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). The concentration of ammonia in the cecal contents was not affected
by the diet. The concentrations of total organic acids and acetic,
propionic and lactic acids in the cecal contents were not affected by
the diet. However, the concentration of n-butyric acid in
the cecal contents was significantly lower in the rats fed the LS or HS
diets than in the control rats. The concentration of succinic acid in
the cecal contents of rats fed the HS-HC diet was significantly
lower than that in the control rats.
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). The plasma cholesterol concentration in the rats fed the HS-HC
diet was significantly lower than that in the control rats and was
significantly lower than that in the rats fed the LS diets. The plasma
triglyceride concentration, the liver weight and concentrations of
liver total lipids, cholesterol and triglyceride were not affected by
the diet (data not shown). The levels of bile acids in the cecal
contents and fecal excretion of bile acids were higher in the rats fed
the HS diets than in the control rats and in the rats fed the LS diets.
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). However, the apparent absorption of Zn in the rats fed the HS-MC
or HS-HC diet was significantly lower than that in the control rats
and in the rats fed the LS diets. The apparent absorption of Fe in the
rats fed the LS or HS diets was significantly lower than that in the
control rats. The apparent absorption of Fe slowly decreased with
increasing DC. The apparent absorption of Fe in the rats fed the HS
diets was significantly lower than that in the rats fed the LS-LC
or LS-MC diet.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, 19
). On the other hand, it has been
reported that cross-linking with phosphate has no effect on the in
vivo digestibility of HDP from tapioca starch (20)
or
potato starch (1)
. In the present study, the level of
amylase-resistant starch in HS was more than twice as great
as that in LS with the respective DC; however, the level of
amylase-resistant starch was only slightly affected by the DC in
the HDP.
A summary of investigations concerning the in vivo digestibility of
various CMS was published by FAO/WHO (21)
. In some
studies, reduced digestibility, often in association with diarrhea and
cecal enlargement, was observed after modification of starches,
particularly at high levels of intake. We previously reported that the
severity of diarrhea increased with increasing DS and with increasing
DC in rats fed hydroxypropylated potato starch or HDP (DS = 0.01)
from potato starch at 100 g/kg (19)
. In the present study,
diarrhea was observed in the rats fed all LS and HS diets, but the
degree of diarrhea was not affected by the DS. Cecal enlargement was
observed in the rats fed the HS diets but not in the rats fed the LS
diets. However, among the rats fed the HS diets, the degree of cecal
enlargement was not affected by the DC. It has been demonstrated that
enlargement of the cecum is due to an increased load of osmotically
active substances in the caudal part of the intestinal tract
(22
, 23
). In the case of carbohydrates, it
would primarily be associated with short-chain fatty acids (SCFA)
produced by the gut microflora from the undigested part of the
carbohydrate. However, the SCFA concentration in the cecum of the rats
fed the LS and HS diets did not significantly differ from that in the
control rats. On the other hand, Oku et al. (24)
speculated that cecal enlargement depends on the amount of maldigested
materials that reach the cecum. The level of amylase-resistant
starch in the HS diet was greater than that in the LS diet. The wet
weight of the cecal content of the rats fed the HS diet was
significantly greater than that of the control rats; however, the wet
weight of the cecal content of the rats fed the LS diet was not.
Therefore, the cecal enlargement caused by the HS diet may be due to
increased influx of the unabsorbed starch fraction into the cecum. The
cecal tissue weight of the rats fed the HS diet was heavier than that
in the control rats. Til et al. (25)
showed that feeding
HDP (DS = 0.075) from potato starch led to an increase in the
tissue weight of the cecum. Feeding nonfermentable bulk to rats
predominantly increased the thickness of the muscularis externa
(26)
. There was a positive correlation between the cecal
content and cecal tissue weight among rats fed diets containing
resistant starch (27)
. Thus, the increase in cecal content
may have contributed to the heavier cecal tissue weight in the rats fed
the HS diet. Til et al. (25)
showed that feeding HDP (DS
= 0.075) from potato starch leads to an increase in the weight of
the colon. However, in the present study, the LS and HS diets did not
lead to an increase in the colon tissue weight. Enlargement of the
large intestine is known to readily occur in rats fed CMS
(28)
.
The apparent protein digestibility in the rats fed the HS-MC or
HS-HC diet was lower than that in the control rats. A reduction in
feed efficiency is generally caused by reduced digestibility of
proteins and/or energy sources and by reduced retention of nutrients
resulting from various metabolic disturbances. However, the feed
efficiency and body mass gain in the rats fed the HS-MC or
HS-HC diet did not differ from those in the control rats. Thus, it
does not appear that HS-MC and HS-HC interfere with the
digestion and absorption of protein and energy sources. On the other
hand, the fecal N excretion (data not shown) and fecal output were
greater in the rats fed the HS-MC or HS-HC diet than in the
control rats. The greater fecal N excretion is caused by reduced
protein digestibility and by increased production of endogenous protein
(e.g., digestive enzymes and sloughed cells) and/or by greater fecal
biomass. The bacteria in the large bowel play a major role in fecal
bulking and constitute a large proportion of fecal N (29)
.
However, the amylase-resistant starch in HDP is not a good
substrate for bacteria in the large bowel (1
,
30
). Thus, the greater fecal N excretion and the lower
apparent protein digestibility in the rats fed the HS-MC or
HS-HC diet may be due to increased fecal output as a result of a
shorter transit time in the large bowel.
The fecal wet weights and fecal moistures in the rats fed the LS-HC and HS diets were significantly greater than those of the control rats, but those in the rats fed the LS-LC or LS-MC diet were not. If the magnitude of the laxative effect is calculated as the increase in fecal wet weight per gram of amylase-resistant starch consumed, the effect was as follows (g/g): 0.028 for the LS-LC diet, 0.049 for the LS-MC diet, 0.289 for the LS-HC diet, 0.835 for the HS-LC diet, 1.267 for the HS-MC diet and 1.310 for the HS-HC diet. The laxative effect of the LS and HS diets increased as the level of amylase-resistant starch increased (r = 0.969, P = 0.0014). Therefore, the increase in fecal output in the rats fed LS-HC and HS diets is due to the increases in fecal moisture and level of amylase-resistant starch. The amount of absorbed moisture in the colon of rats fed the LS-HC and LS diets was significantly lower than that in the control rats. The contents in the colon of the rats fed the LS-HC and HS diets felt stickier and more viscous to the touch compared with those of the rats fed the TS diet. Therefore, the reduced moisture absorption in the colon of rats fed the LS-HC and HS diets would be due to inhibition of diffusion.
The plasma cholesterol concentration in the rats fed the HS-HC diet
was significantly lower than that in the control rats, and that in the
rats fed the HS-LC or HS-MC diet was slightly (P
= 0.097) but not significantly lower than that in the control
rats. Because the experimental diets were not supplemented with
cholesterol, the hypocholesterolemic effect of the HS diet must involve
changes in endogenous sterol metabolism. One possibility is increased
fecal excretion of cholesterol and bile acids. Bile acids may bind to
HS in the small intestine, because starch has been shown to bind bile
acids in vitro (31)
. The cecal contents and fecal
excretion of bile acids in the rats fed the HS diet were significantly
larger than the respective values in the rats fed the LS diet. By
inhibiting the reabsorption of bile acids and enhancing fecal bile acid
excretion, the HS may cause increased hepatic synthesis of bile acids,
thereby reducing the serum cholesterol concentration. However, it is
still unclear whether each type of HS can effectively bind bile acids.
Another possible explanation concerns propionic acid production from
fermentation of HS in the large bowel. When propionic acid was
fed to rats, it significantly reduced the serum cholesterol
concentration (32)
. Propionic acid infused into the cecum
prevented the increase in plasma cholesterol concentration in rats fed
a cholesterol-free casein diet (33)
. Furthermore, in
vitro studies using rat liver cells have shown that propionic acid may
attenuate hepatic cholesterol synthesis (34)
. On the other
hand, other studies have shown that propionic acid has no
hypocholesterolemic effects (35
, 36
).
However, in the present study, the concentration of propionic acid in
the cecal content was not affected by the diet. Further studies are
needed to elucidate the mechanism of the hypocholesterolemic effect of
HS.
A strong negative correlation has been found between the cecal pH and
the cecal pool of SCFA (37)
. However, despite a similar
cecal pool size of organic acids, the cecal pH in the rats fed the HS
diet was lower than that in the control rats. Lactic acid is poorly and
slowly absorbed (38
, 39
). Hoshi et al.
(40)
suggested that the higher concentration of cecal
succinic acid predominantly appears to contribute to the lower cecal
pH. However, in the present study, the concentration of lactic acid was
not affected by the diet. Moreover, the concentration of succinic acid
in the rats fed HS-HC diet was lower than that in the control rats.
A recent in vitro study examined carbohydrate fermentation in human
fecal slurries and found that starch fermentation increased
n-butyric acid production (41
,
42
). In the present study, the LS and HS diets did not
increase the concentration of n-butyric acid compared with
that in the control rats. Also, the LS and HS diets did not increase
the concentration of propionic acid in comparison with that
in the control rats. These are in agreement with the result of our
previous study in rats fed HDP (DS = 0.01, 100 g/kg diet) from
potato starch (19)
. The lower concentration of
n-butyric acid can be explained by the cecal enlargement,
because butyric acid is readily oxidized by cecal and colonic
epithelial cells (43)
. Also, this lower concentration of
n-butyric acid can be explained by the lower concentration
of butyric acid–producing bacteria. The amylase-resistant starch
in LS and HS may not be a good substrate for butyric acid–producing
bacteria. The concentration of acetic, lactic or succinic acid in the
rats fed the LS or HS diet was not higher than that in the control
rats. However, in a previous study, we found that rats that were fed
HDP (100 g/kg diet) with a molar substitution of 0.01 from potato
starch had higher concentrations of acetic, lactic and succinic acids
than the control rats fed potato starch (19)
. On the other
hand, it has been reported that the pancreatin-indigested fractions
in HDP are not good substrates for lactic acid–producing bacteria in
in vitro bacterial fermentation (30)
. The apparent
digestibility of CMS and the structure of the maldigested fraction in
feces after CMS administration depend on the type of modification
(1)
. Therefore, the difference in the results between the
present study and our previous study is due to the differences in the
quality and quantity of HDP.
The apparent absorptions of Ca and Mg were not affected by the diet.
Mineral absorption generally occurs in the upper part of the intestine.
However, in rats, the large intestine has a high capacity for Mg and Ca
absorption (44)
. Moreover, it has been reported that SCFA
also contribute to enhance the absorption of Ca and Mg from the cecum
(45
46
47)
. On the other hand, the apparent absorption of Zn
in the rats fed the HS diet was significantly lower than that in the
control rats, but the apparent absorption of Zn in the rats fed the LS
diet was not. The apparent absorption of Fe in the rats fed the LS or
HS diet was significantly lower than that in the control rats. Bruns
and Hood (48)
reported that HDP bound iron in vitro. Hood
et al. (49)
reported that feeding HDP resulted in marked
depression in iron retention in iron-deficient rats.
These results show that the characteristics of amylase-resistant starch in HDP are similar to dietary fiber, with respect to increases fecal bulking and fecal excretion of bile acids, an change in pH of cecal content, decreases in absorption of Fe and Zn and an decrease in apparent protein digestibility. The dietary fiber–like effects of CMS would be affected by the type of modification. In fact, dietary fiber–like effects of HDP depend on the DS but not the DC.
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FOOTNOTES |
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Manuscript received July 17, 2000. Initial review completed August 11, 2000. Revision accepted October 20, 2000.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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