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Articles

Heat Moisture Treatment of High Amylose Cornstarch Increases Its Resistant Starch Content but Not Its Physiologic Effects in Rats¹

Department of Biological Resources, Faculty of Agriculture, Ehime University, Matsuyama 790, Japan

²To whom correspondence should be addressed. E-mail: ebihara{at}agr.ehime-u.ac.jp.

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
To examine whether the physiologic effects of high amylose cornstarch (HACS) are affected by gelatinization or heat moisture treatment, male rats were fed for 21 d a fiber-free purified diet containing 40 g/100 g gelatinized normal cornstarch (G-CS), HACS, gelatinized high amylose cornstarch (G-HACS) or heat moisture–treated HACS (HMCS). Dietary fiber (DF) content in G-HACS was 87% lower than that in HACS. The apparent starch and protein digestibilities were higher in the G-HACS group than in the HACS group. Fecal wet weight and fecal bile acid excretion were lower in the G-HACS group than in the HACS group. The cecal tissue weight, cecal surface area, cecal content weight and cecal pH were lower in the G-HACS group than in the HACS group. The cecal n-butyric acid and succinic acid concentrations were higher and lower, respectively, in the G-HACS group than in the HACS group. The plasma cholesterol and triacylglycerol concentrations did not differ between the G-HACS group and the HACS group. On the other hand, the DF content in HMCS was 330% higher than that in HACS, but the HMCS and HACS groups generally did not differ except in cecal surface area. Dietary starch did not affect fecal moisture, fecal neutral sterol (cholesterol + coprostanol) excretion, liver cholesterol level, total short-chain fatty acid (SCFA) concentration or apparent Ca, Fe, Mg and Zn absorptions. These results show that the heat moisture treatment of HACS for the most part does not alter its physiologic effects despite the greater DF content.

KEY WORDS: • high amylose cornstarch • heat moisture treatment • gelatinization • physiologic effect • rats

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Resistant starch (RS)³ is, by definition, that sum of starch and the products of starch degradation not absorbed in the small intestine of healthy individuals (1) . By the standard American Association of Cereal Chemists method for determining dietary fiber (DF) (2) , RS is an insoluble DF (3) . RS that escapes hydrolysis in the small intestine enters the large intestine where it is fermented (4) . In this regard, RS possesses physiologic properties similar to those of DF. The DF-like functional characteristics of RS make it desirable for use in some foods. The supplementation of RS into foods may help overcome the present deficiency of DF in the Western diet. RS may have beneficial effects on intestinal function and may aid in preventing Western diseases.

High amylose cornstarch (HACS) contains type-2 RS, ungelatinized starch granules that are highly resistant to digestion by -amylase until gelatinized. Unlike DF, supplementation of HACS into foods does not adversely affect the taste and texture of foods (5) . Moreover, a potential advantage of using HACS is the facility with which its content in foods can be modified by choosing the appropriate raw materials and processing conditions (6 –8) . HACS offers a major advantage because it can be technologically processed to alter the apparent DF content of foods without greatly changing their organoleptic properties.

It has been reported that HACS reduces plasma cholesterol and triacylglycerol concentrations (9 –11) . Mathe et al. (12) found that HACS reduced the plasma cholesterol concentration in genetically obese and lean Zucker rats. The plasma cholesterol and triacylglycerol concentrations were reduced as the dietary level of HACS increased in rats (13) .

HACS and modified HACS such as gelatinized HACS (G-HACS) and heat moisture–treated HACS (HMCS) are used by the food industry to improve the physical properties of various food items (5 ,14) . Their consumption is increasing as the consumption of processed foods increases. The susceptibility of HACS to pancreatic -amylase and the formation of RS were decreased and increased, respectively, by heat moisture treatment (15) . The physiologic effects of consuming HACS are considered to be due to the physicochemical properties of RS. Therefore, we studied the physiologic effects of consuming HACS, G-HACS and HMCS. Gelatinized normal cornstarch (G-CS) was used as a reference.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Materials.

G-CS (Nisshoku Corn Starch Y), HACS (Nisshoku High Amylose Starch), G-HACS (Nisshoku Alstar H) and HMCS (Nisshoku Lodestar) were purchased from Nihon Shokuhin Kako (Tokyo, Japan). The DF contents of HACS, G-HACS and HMCS as determined by the method of the AOAC (16) were 19.3, 2.4 and 64.5 g/100 g, respectively. DF was not detected in G-CS. The amylose contents of G-CS and HACS were 26 and 68 g/100 g, respectively.

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 (6 wk old; Japan SLC, Hamamatsu, Japan) weighing 120–140 g were used in this study. The rats were housed individually in cages with stainless steel screen bottoms in a room with controlled temperature (22–24°C) and lighting (lights on, 0700–1900h). The rats were acclimated by feeding a commercial solid diet (MF, oriental Yeast, Osaka, Japan) for 7 d. After acclimation, 24 rats weighing 170–180 g were divided into four groups (n = 6) and were allowed free access to the G-CS, HACS, G-HACS or HMCS diets (Table 1) for 21 d. Body weight and food intake were recorded daily for each rat in the morning before replacing the diet.

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 concentration of nitrogen (N) in the diet consumed by the rat during the final 3 d and that in the feces were analyzed in duplicate for each collection by the Kjeldahl method (18) . The apparent digestibility of protein (N x 6.25) was calculated by measuring the N content in the diet consumed by the rat during the final 3 d and that in the feces. The concentrations of starch in the diet consumed by the rat during the last 3 d and that in the feces were measured in duplicate for each collection with the Megazyme Total Starch Assay Kit (Megazyme Australia, Sydney, Australia) using a modification that involves preheating the samples in dimethyl sulfoxide at 100°C for 30 min (19) . The apparent digestibility of starch was calculated as the difference between the dietary intake and fecal excretion of starch.

To determine the concentrations of Ca, Fe, Mg and Zn, 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/L lanthanum chloride. The apparent absorptions of Ca, Fe, Mg or Zn were calculated as the difference between the dietary intake and fecal excretion.

Fecal steroids were extracted with a mixture of chloroform/methanol (1:1, v/v) at 70°C for 60 h (20) . The concentration of fecal total bile acids was determined enzymatically by the 3-hydroxysteroid dehydrogenase assay method of Sheltaway and Losowsky (21) using taurocholic acid as the standard. The analyses of fecal neutral sterols, cholesterol and coprostanol were performed by gas-liquid chromatography (Model HP5890A, Hewlett-Packard, Palo Alto, CA) equipped with a flame-ionization detector and a capillary column coated with DB-1 (J&W Scientific, Folsom, CA; 30 m x 0.53 mm i.d.; 3-µm film thickness). The oven temperature was 260°C, and the flow rate of the carrier gas, helium, was 3.8 mL/min. 5-Cholestane was used as the internal standard.

Blood was collected from the abdominal aorta at midnight from fed rats that were under sodium pentobarbital (50 mg/kg body; Nembutal, Abbot Laboratories, North Chicago, IL) anesthesia. Blood collection tubes (Vacutainer, Becton Dickinson, Franklin Lakes, NJ) 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 contents was determined as the difference between the wet mass and the dry mass of the cecal contents 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/L NaCl, 4°C), blotted on filter paper and weighed. The surface area of the cecum was estimated by pinning it flat on a sheet of paper (of known weight per surface area) and then trimming and weighing the paper (22) . Measurement of cecal organic acids was performed as described previously (23) .

The triacylglycerol and total cholesterol concentrations in the plasma were determined enzymatically with commercial kits (Triglyceride E-Test Wako and Cholesterol E Test Wako, Wako Pure Chemical, Osaka, Japan). The concentration of liver total lipids was determined gravimetrically after extraction by the method of Folch et al. (24) . The concentrations of liver triacylglycerol 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. (24) . After extraction, the volume of the lipid solution was adjusted to 20 mL with the same solution of chloroform/methanol (2:1, v/v). The extract (1 mL) was dried under a nitrogen stream and the residue obtained was mixed with 100 µL isopropyl alcohol containing 100 g Triton X-100/L (Wako Pure Chemical). This mixture (30 µL) 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), and the triacylglycerol 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 among groups was evaluated with one-way ANOVA followed by Duncan’s new multiple range test using the SuperANOVA statistical software package (Abacus Concepts, Berkeley, CA). The significance of relationships between variables was established by linear or logarithmic regression analysis using the Laleida Graph program (Synergy Software, Reading, PA). Differences were considered to be significant at P < 0.05.

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Although the food intake of rats fed the HMCS diet was significantly less than that of rats fed the G-CS diet, there were no significant differences in body weight gain among the four groups of rats (Table 2). Food efficiency was not affected by diet. The apparent starch and protein digestibilities in rats fed the HACS and HMCS diets were significantly lower than those in rats fed the G-CS and G-HACS diets. The apparent protein digestibility in rats fed the G-HACS diet was significantly lower than that in rats fed the G-CS diet. The apparent absorptions of Ca, Fe, Mg and Zn were not affected by diet.

(Table 3

(Table 4

(Table 5

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

The plasma total cholesterol concentrations in rats fed the HACS, G-HACS and HMCS diets were significantly lower than that in rats fed the G-CS diet (Table 3) . One possible explanation is increased fecal steroid excretion. The fecal excretion of bile acids in rats fed the HACS diet was significantly higher than that in rats fed the G-CS diet, but that in rats fed the HMCS diet was not. The fecal excretion of neutral sterols was not affected by diet. These findings suggest that the increase in fecal steroid excretion is not necessarily a primary mediator of the hypocholesterolemic effect of HACS or HMCS.

Another possible explanation is a rise in the intestinal pool and biliary excretion of bile acids. In this study, we did not measure the amount of bile acids in the small intestine or the biliary excretion of bile acids. However, in another experiment, we measured them in rats fed a diet containing 200 g HACS/kg diet for 21 d. The small intestinal bile acid pool in rats fed the 20% HACS diet was 160% greater than that in the rats fed the G-CS diet (unpublished data). The biliary excretion of bile acids in rats fed the 20% HACS diet was 40% higher than that in the rats fed the G-CS diet (unpublished data). Therefore, the hypocholesterolemic effects of HACS and HMCS appear to be mediated by a rise in the intestinal pool and biliary production of bile acids. The cholesterol concentrations in the LDL + VLDL fraction in rats fed the HACS and HMCS diets were significantly lower than that in rats fed the G-CS diet. In this study, the rats were killed in the fed state; thus, the LDL + VLDL fraction would contain chylomicrons. This could explain at least part of the rather large differences in plasma cholesterol among the groups. On the other hand, in humans, Heijnen et al. (32) did not find any plasma lipid-lowering effect when giving 30 g HACS/d to healthy, normolipidemic subjects. The effects demonstrated in rats (9 –13) probably will require higher doses of HACS than are feasible in a human diet.

The plasma triacylglycerol concentrations in rats fed the HACS and HMCS diets were significantly lower than that in rats fed the G-CS diet (Table 3) . It has been reported that the postprandial glucose and insulin responses are larger in rats fed normal cornstarch than in rats fed HACS (33) . Feeding a diet rich in amylose may produce a lower glycemic response and a lower rate of gastric emptying, consequently leading to reductions in lipogenesis in adipose tissue and in liver (34) . It seems that larger postprandial glucose and insulin responses would increase the biosyntheses of fatty acids and triacylglycerols. Therefore, HACS and HMCS may inhibit the increase in plasma triacylglycerol concentration by suppressing the rapid increase in postprandial glucose. The plasma triacylglycerol concentration and the amount of RS were correlated logarithmically (r = -0.965, P < 0.02), suggesting a saturation of plasma triacylglycerol concentration with increasing dietary levels of DF.

The HACS and HMCS diets elicited marked enlargements of the cecum compared with the G-CS and G-HACS diets (Table 4) . 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 (35 ,36) . In the case of carbohydrates, enlargement of the cecum would be associated primarily with the SCFA produced by gut microflora from the nondigested part of the carbohydrate. However, the total SCFA concentrations in the cecal contents of rats fed the HACS and HMCS diets did not differ significantly from those in rats fed the G-CS and G-HACS diets. On the other hand, Oku et al. (37) speculated that cecal enlargement depends on the amount of maldigested materials that reach the cecum. The wet weights of the cecal contents of rats fed the HACS and HMCS diet were 360 and 460% greater, respectively, than that of rats fed the G-CS diet, and 49 and 81% greater, respectively, than that of rats fed the G-HACS diet. Therefore, the cecal enlargement caused by the HACS and HMCS diets may be due to increased influx of the unabsorbed starch fraction into the cecum. The cecal tissue weights of rats fed the HACS, G-HACS and HMCS diets were 137, 73 and 144% greater, respectively, than that in the rats fed the G-CS diet. Feeding nonfermentable bulk to rats predominantly increases the thickness of the muscularis external (38) . There was a positive correlation between the weight of the cecal contents and cecal tissue weights among rats fed diets containing RS (39) . In the present study, there was a positive correlation between the weight of the cecal contents and cecal tissue weight (r = 0.988, P < 0.02). Thus, the increase in cecal contents may have contributed to the heavier cecal tissue weight in rats fed the HACS, G-HACS and HMCS diets.

The cecal pH of rats fed the HACS and HMCS diets were significantly lower than those of rats fed the G-CS and G-HACS diets, and that of the rats fed the G-HACS diet was significantly lower than that of the rats fed the G-CS diet. The total SCFA concentration in the cecal contents was not affected by diet. However, the concentration of succinic + lactic acids in the cecal contents decreased in the following order: rats fed the HACS diet > rats fed the HMCS diet > rats fed the G-HACS diet > rats fed the G-CS diet. Lactic acid is poorly and slowly absorbed (40 ,41) . Hoshi et al. (42) suggested that a high concentration of cecal succinic acid contributes predominantly to low cecal pH. There was a negative correlation between the cecal pH and the cecal succinic acid concentration in the present study (r = -0.978, P < 0.05). Therefore, it appears that the lower cecal pH in rats fed the HACS, G-HACS and HMCS diets depended on the higher concentration of succinic + lactic acids in the cecal contents.

The cecal concentration of succinic acid in rats fed the HACS and HMCS diets were significantly higher than that in rats fed the G-CS and G-HACS diets; however, the reason for this is uncertain. Succinic acid is a normal product of microbial fermentation in the large intestine and is an intermediate in the synthesis of propionic acid (43) . However, in the present study, the lower cecal concentration of succinic acid in rats fed the G-CS and G-HACS diets was not accompanied by any significant change in the cecal concentration of propionic acid. The cecal concentration of succinic acid was negatively correlated with the cecal concentration of n-butyric acid (r = -0989, P < 0.02). The cecal concentration of succinic acid tended to increase with increasing cecal contents (P = 0.06). The differences in fermentation profiles may be due to differences in cecal microflora and/or the amount of undigested materials flowing into the cecum. The coprostanol/cholesterol ratio in the feces was significantly lower in rats fed the HACS and HMCS diets than in those fed the G-CS and G-HACS diets (Table 5) , suggesting that HACS and HMCS may alter the relative proportion of cecal bacterial species. Moreover, HACS and HMCS may be good substrates for succinic acid–producing bacteria, but may not be good substrates for n-butyric acid–producing bacteria.

The fecal wet weights in rats fed the HACS and HMCS diets were significantly greater than those in rats fed the G-CS and G-HACS diets (Table 5) . Increased fecal wet weight can be attributed to water, undigested starch, bacterial mass and protein excretion. Indeed, the fecal wet weight was positively correlated with the apparent starch digestibility (r = 0.991, P < 0.01), and tended to be correlated with the apparent protein digestibility (r = 0.928, P = 0.07). Fecal moisture was not affected by diet. Brown et al. (44) also reported that in pigs fed high amylose cornstarch, the fecal output was higher but the moisture content of the feces was not affected. If the magnitude of the laxative effect is calculated as the increase in fecal wet weight per gram of HACS, HMCS or G-HACS consumed in comparison with that of G-CS, the effect was as follows (g/g): 0.285 for the HACS diet, 0.409 for the HMCS diet and 0.076 for the G-HACS diet. The laxative effect exponentially increased as the DF content increased.

The HMCS and HACS groups showed similar results in most of the physiologic variables. Therefore, this study shows that although the DF content in HACS increased by heat moisture treatment, such treatment of HACS for the most part does not affect its physiologic effects.

	FOOTNOTES

 
¹ Supported in part by Elizabeth Arnold Fuji Foundation.

³ Abbreviations used: DF, dietary fiber; G-CS, gelatinized normal cornstarch; G-HACS, gelatinized high amylose cornstarch; HACS, high amylose cornstarch; HMCS, heat moisture–treated high amylose cornstarch; RS, resistant starch; SCFA, short-chain fatty acid.

Manuscript received January 29, 2001. Initial review completed March 13, 2001. Revision accepted June 20, 2001.

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TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 

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