摘要
目的
抗性淀粉(Resistant Starch,RS)是一种“不被健康人体小肠所吸收的淀粉及其分解物的总称”。国内外研究发现,抗性淀粉通过在结肠内发酵产生有益的发酵产物促进肠道健康,抗性淀粉还能改善脂代谢以及控制餐后血糖和胰岛素升高,因此人们认为抗性淀粉是一种功能性的食物成分。转双反义SBE基因水稻是一种富含抗性淀粉的水稻,本研究将通过动物实验和人体实验对该转基因水稻的食用安全性及功效进行研究。
材料与方法
1.转双反义SBE基因水稻亚慢性毒性实验(90天喂养实验)
初断乳Wistar大鼠100只,雌雄比例1:1,体重80g～90g,适应7天后按体重随机分为5组,每组20只,雌雄各半。分别喂饲亲本大米高剂量掺入饲料(No-GM)、转基因大米高剂量掺入饲料(GM)、转基因大米中剂量掺入饲料(Half-GM)、转基因大米低剂量掺入饲料(Quarter-GM)和AIN-93G正常对照饲料(ND)。所有动物自由进食饮水。每周称量2次进食量,1次体重。实验中期和实验结束时各检测血常规和血生化1次。90天后处死大鼠,取右股骨测量骨密度;取脑、心、肝、脾、肾、睾丸(或子宫)、胸腺称重,计算脏器系数;上述脏器及胃、十二指肠、空肠、回肠、盲肠、结肠和直肠等要进行常规病理学检查。
2.转双反义SBE基因水稻对大鼠肠道健康的影响
健康成年雄性SD大鼠48只,体重210g～230g,适应7天后按体重随机分为4组,每组12只。分别喂饲亲本大米高剂量掺入饲料(No-GM)、转基因大米高剂量掺入饲料(GM)、转基因大米中剂量掺入饲料(Half-GM)和AIN-93M正常对照饲料(ND)。喂养5周后连续收集4天新鲜粪便,测定粪便重量、水分、干重、pH值和短链脂肪酸含量,6周后处死大鼠并收集盲肠、结肠内容物,测定内容物和肠壁重量、内容物pH值和短链脂肪酸含量。
3.转双反义SBE基因水稻预防高脂饲料诱导的大鼠血脂异常
健康成年雄性SD大鼠50只,体重210g～230g,适应7天后按体重随机分为5组,每组10只。分别喂饲亲本大米高剂量掺入高脂饲料(NoGM-HF)、转基因大米高剂量掺入高脂饲料(GM-HF)、转基因大米中剂量掺入高脂饲料(HGM-HF)、高脂饲料(HF)和AIN-93M正常对照饲料(ND)。所有动物每天定量给予各组饲料,分别于实验开始后第4周、第8周、第13周取血,分离血清测定甘油三酯、胆固醇、高密度脂蛋白胆固醇含量。13周后处死大鼠并收集肝脏,测定肝脏甘油三酯和胆固醇含量。
4.转双反义SBE基因水稻重要营养素消化率的体内实验研究
五指山小型去势公猪8只,体重30kg～35kg。术前单个放入代谢笼内适应喂养7天,期间用通灭(多拉菌素注射液)行肠道驱虫处理。7天后,动物禁食36小时,禁水12小时,进行回肠造瘘手术。手术后2周,选择7只恢复良好的小型猪作为实验对象,将小型猪分为两组,采用交叉法分别喂饲转基因大米饲料和亲本大米饲料,饲料中加入三氧化二铬作为指示剂。每种饲料适应喂养4天后连续收集3天的食糜,然后换另一种饲料,重复上述步骤。最后统一喂饲5%酪蛋白饲料以测定内源性氨基酸的排出量。食糜收集后用均浆机混匀,冷冻干燥后再次混匀过60目筛子,分析两种大米食糜中主要营养素含量并计算消化率。采用氨基酸评分和经蛋白质消化率校正的氨基酸评分评价两种大米的蛋白质质量。实验结束后处死小型猪,并取瘘管处肠段及瘘管处上下肠段进行病理检测。
5.转双反义SBE基因水稻餐后血糖和胰岛素效应以及在人体大肠中发酵情况的研究
男女各10名受试者参加本实验,经过常规体检和葡萄糖耐量实验筛选后,合格受试者16名(9名男受试者平均年龄24.3±1.0,7名女受试者平均年龄24.6±1.0),将男女各分为3组采用交叉设计分别食用40g葡萄糖、相当于40g碳水化物的转基因大米和亲本大米蒸煮后的米饭,洗脱期为1周,3周内交叉食用受试物。受试者于实验当天上午6点到达实验室,静坐半小时后,于前臂静脉埋入静脉留置针收集空腹血样,分别于餐后15min、30min、45min、60min、90min、120min、180min和240min采取静脉血2mL(血糖专用的血液收集管),分离血浆-20℃保存备检。食用转基因大米和亲本大米米饭前先测定空腹呼气中氢气含量,餐后3.5h～14h每隔半小时测定1次,14h～16h每隔1小时测定1次,至16小时结束。由于要监测食用两种米饭后16小时内呼气中氢气含量,因此受试者实验前1天晚餐和实验当天的午餐及晚餐的种类和数量要统一安排,避免产氢食物,如乳制品、麦面制品和豆类制品。
结果
1.转双反义SBE基因水稻亚慢性毒性实验(90天喂养实验)
各组大鼠平均每日摄食量之间的差异和体重之间的差异均没有显著性(P＞0.05)。实验中期,雌性大鼠转基因大米GM组平均红细胞容积显著高于亲本大米No-GM组(P＜0.05),单核细胞百分比显著低于ND对照组(P＜0.05),谷草转氨酶活性显著高于ND对照组(P＜0.05)。雌性大鼠转基因大米Half-GM组谷丙转氨酶活性显著高于亲本大米No-GM组和ND对照组。雄性大鼠转基因大米GM组平均红细胞容积显著高于ND对照组(P＜0.05)。实验末期,雌性大鼠转基因大米GM组平均红细胞血红蛋白量显著高于亲本大米No-GM组(P＜0.05),谷丙转氨酶和谷草转氨酶活性高于ND对照组。雄性大鼠转基因大米GM组红细胞压积和尿素氮显著低于亲本大米No-GM组(P＜0.05),单核细胞百分比显著高于ND对照组(P＜0.05)。
转基因大米GM组雌性大鼠大脑的脏器系数显著大于亲本大米No-GM组(P＜0.05),转基因大米GM、Half-GM、Quarter-GM组雌性大鼠肾脏脏器系数显著小于ND对照组(P＜0.05)。实验大鼠各组之间血脂、血钙和骨密度均无统计学差异,内脏病理检查未发现明显异常。
2.转双反义SBE基因水稻对大鼠肠道健康的影响
转基因大米GM组大鼠体重增长趋势接近ND对照组大鼠,显著低于No-GM组大鼠体重的增长(P＜0.05)。与No-GM组和ND对照组大鼠相比,转基因大米GM组和Half-GM组粪便量、粪便水分、盲肠壁以及内容物含量显著增加(P＜0.05),并且上述指标在GM组和Half-GM组之间的差异也存在显著性(P＜0.05)。GM组结肠壁重量显著高于No-GM组和ND对照组(P＜0.05)。各组大鼠盲肠、结肠和粪便中短链脂肪酸的含量逐渐降低,除了Half-GM组结肠中丁酸含量与其他各组的差异没有显著性外,GM组和Half-GM组盲肠、结肠中短链脂肪酸的含量与No-GM组和ND对照组相比都有显著增加(P＜0.05),各组大鼠粪便中丁酸含量的差异消失,但是乙酸和丙酸含量的差异仍然存在(P＜0.05)。GM组和Half-GM组大鼠粪便和盲肠的pH值显著低于No-GM组和ND对照组(P＜0.05)。
3.转双反义SBE基因水稻预防高脂饲料诱导的大鼠血脂异常
实验前各组大鼠体重的差异和每日进食量的差异均没有显著性(P＞0.05),实验4周后,NoGM-HF组、GM-HF组、HGM-HF组和HF组大鼠体重均显著高于ND对照组,这种显著性差异一直持续至实验结束。NoGM-HF、GM-HF、HGM-HF和HF组大鼠血清甘油三酯含量在实验进行至13周时与ND对照组相比才出现显著性升高(P＜0.05),但NoGM-HF、GM-HF、HGM-HF和HF组血清甘油三酯之间的差异没有显著性(P＞0.05)。实验4周后,NoGM-HF、GM-HF、HGM-HF和HF组大鼠血清胆固醇之间的差异没有显著性(P＞0.05),但是与ND对照组相比,均有显著性升高(P＜0.05),并且这种显著性差异一直持续至实验结束。大鼠血清HDL-C从实验开始至结束,各组之间的差异均没有显著性(P＞0.05)。实验结束时各组大鼠肝脏胆固醇含量之间以及甘油三酯含量之间的差异也没有显著性(P＞0.05)。
4.转双反义SBE基因水稻重要营养素消化率的体内实验研究
转基因大米中18种氨基酸、蛋白质的表观消化率和真消化率与亲本大米的差异没有显著性,但是转基因大米中碳水化合物和能量的消化率显著低于亲本大米(P＜0.05)。转基因大米和亲本大米的AAS评分分别为75%和62%,PDCAAS评分分别为65%和56%。
5.转双反义SBE基因水稻餐后血糖和胰岛素效应以及在人体大肠中发酵情况的研究
食用转基因米饭和亲本米饭前空腹血糖浓度分别为4.7±0.3mmol/L、4.6±0.4mmol/L,差异没有显著性(P＞0.05);餐后血糖最大值分别为6.8±0.4mmol/L、7.2±0.6mmol/L,存在显著性差异(P＜0.05)。食用转基因米饭后30min、45min、60min、90min和120min的血糖值均显著低于食用亲本米饭后的血糖(P＜0.05)。以葡萄糖GI值为100作为参照,转基因大米的GI值为48.4±21.8,亲本大米GI值为77.4±34.9,两者之间存在显著性差异(P＜0.05)。
食用转基因米饭和亲本米饭前空腹血浆胰岛素浓度分别为6.7±2.3μIU/mL、6.8±2.4μIU/mL,差异没有显著性(P＞0.05)。食用转基因米饭后45min、60min、90min和120min的血浆胰岛素值均显著低于食用亲本米饭后的血浆胰岛素(P＜0.05)。以葡萄糖Ⅱ值为100作为参照,转基因大米的Ⅱ值为34.2±18.9,亲本大米Ⅱ值为54.4±22.4,两者之间存在显著性差异(P＜0.05)。
受试者食用转基因米饭后5h时呼气氢明显升高并维持在较高水平,最高值(38.9±10.5ppm)显著高于食用亲本米饭后呼气氢的最高值(17.6±3.7ppm)(P＜0.05)。食用转基因大米米饭后5h～16h之间各监测点上呼气氢含量均显著高于亲本大米米饭(P＜0.05)。
结论
1.转双反义SBE基因水稻亚慢性毒性实验(90天喂养实验)
虽然个别指标在各组之间存在差异,但是大多数存在差异的指标并没有同时与两个对照组都存在差异;即使在统计学上存在差异显著性的指标,数值相差也不大,大部分在文献报道的范围内。研究认为这些改变应与转基因操作无关,并且病理检查也未发现显著异常,所以现有实验结果不能证实该转基因大米对大鼠有亚慢毒性作用。
2.转双反义SBE基因水稻对大鼠肠道健康的影响
转双反义SBE基因水稻能促进大鼠肠道健康,包括增加粪便体积和水分,增加大肠和粪便中SCFA含量,降低粪便和盲肠pH等。
3.转双反义SBE基因水稻预防高脂饲料诱导的大鼠血脂异常
虽然构建了高脂饲料诱导的大鼠血脂异常模型,但是没有发现转基因大米缓解大鼠血清胆固醇和甘油三酯升高的作用,也未见其改善肝脏脂质的效果。
4.转双反义SBE基因水稻重要营养素消化率的体内实验研究
转基因大米中抗性淀粉含量的增加并没有显著影响到大米中蛋白质、氨基酸的表观消化率和真消化率。由于转基因大米中抗性淀粉保持了在小肠不被吸收的特性,因此转基因大米中碳水化合物和能量消化率显著低于亲本大米。转基因大米AAS评分和PDCAAS评分均略高于亲本大米,因此该转基因大米氨基酸的营养价值和食用价值与亲本大米具有“实质等同性”。
5.转双反义SBE基因水稻餐后血糖和胰岛素效应以及在人体大肠中发酵情况的研究
转双反义SBE基因大米能有效控制餐后血糖和胰岛素升高,并促进其在人体中与发酵相关的产物氢气含量的显著增加。
Objective
Resistant starch (RS) is the sum of starch and products of starch hydrolysis that are not absorbed in the small intestine of healthy individuals. Consumption of RS-enriched foods have shown beneficial effects on the health of large bowel where the RS is fermented by anaerobic bacteria. Resistant starch also can modify lipid metabolism and reduce postprandial glycemic and insulinemic responses. The genetically modified rice with double antisense SBE gene is enriched with resistant starch. This study aimed to evaluate the feeding safety and functional properties of the genetically modified rice through animal and human trials.
Methods
1. Subchronic toxicity test of the genetically modified rice with double antisense SBE gene
100 male and female healthy weanling Wistar rats with an initial weight of 80-90g were randomly sorted into five groups, each consisting of 10 males and 10 females, as follows: No-GM (nongenetically modified rice) group, GM (genetically modified rice) group, Half-GM (half genetically modified rice) group, Quarter-GM (quarter genetically modified rice) group and ND (AIN-93G normal diet) group. During the experiment, food consumption was recorded two times and body weight was measured once in a week. At the middle and end of the experiment, the hematological and biochemical parameters were monitored. At termination, all animals were anaesthetized and killed by exsanguination for gross and histopathological examinations. The main organs were weighed: brain, heart, liver, spleen, kidneys, testicle, uterus, thymus. The organ coefficients were measured and the right legs were isolated for bone density testing.
2. Effects of the genetically modified rice with double antisense SBE gene on the large bowel health in rats
Forty-eight healthy and adult male SD rats with an initial weight of 210-230g were randomly assigned into four groups as follows: No-GM (nongenetically modified rice) group, GM (genetically modified rice) group, Half-GM (half genetically modified rice) group, and ND (AIN-93M normal diet) group. After five weeks, 4-day faecal samples were collected. After six weeks, all animals were anaesthetized and killed by exsanguination. Contents of cecum and colon were collected. Large bowel function was evaluated by determining many indexes related with large bowel health, such as the weight of cecum, colon and their contents, pH and short-chain fatty acid concentration of the contents and feces.
3. The preventive effects of the genetically modified rice with double antisense SBE gene on high fat diet induced blood lipids abnormalities in rats
Fifty healthy and adult male SD rats with an initial weight of 210-230g were randomly divided into five groups as follows: NoGM-HF (nongenetically modified rice with high fat) group, GM-HF (genetically modified rice with high fat) group, HGM-HF( half genetically modified rice with high fat) group, HF (high fat diet) group and ND (AIN-93M normal diet) group. All rats were given equal amount of individual diets every day and at 4w, 8w, 13w after the experiment, serum TG、TC and HDL-C were measured. At 13w, all animals were anaesthetized and killed by exsanguination. Liver lipids including TG and TC were also measured.
4. Study on the digestibility of important nutrients in the genetically modified rice with double antisense SBE gene in vivo
Eight Wuzhishan healthy adult barrows with an initial weight of 30-35kg were housed in adjustable metabolism cages. Pigs were injected with Doramectin injection which is indicated for the treatment and control of the following endoparasites and ectoparasites in cattle during the 7-day adaptation period. After adaptation, pigs were surgically fitted with a simple T-cannula at the terminal ileum. After surgery, seven pigs were chosen as experimental animals. Three diets were prepared. Diet 1 and diet 2 mainly contained nongenetically modified rice and genetically modified rice, respectively. A low-protein (5% casein) diet (diet 3) was fed to determine endogenous amino acid losses. Chromic oxide (0.3%) was includes in all diets as an inert marker. The whole experiment contained three periods. In the first period, four pigs were fed diet 1, the other three pigs were fed diet 2. In second period, diets 1 and diet 2 were exchanged to feed the seven pigs. At last period, all pigs were fed diet 3. Each experimental period lasted seven days. The initial 4-day of each period were considered an adaptation period to the diet. Ileal digesta were collected for 12 h on the last 3-day of the each period. Digesta was immediately frozen at -20℃to prevent microbial degradation of the amino acid in the digesta. At the end of the experiment, ileal digesta were thawed, freeze-dried and ground through a 0.2 mm screen before analysis. At termination, all animals were anaesthetized and killed by exsanguination for determining whether cannulation had caused intestinal abnormalities.
5. Postprandial glycemic and insulinemic responses to genetically modified rice with double antisense SBE gene and its fermentation in the large bowel of healthy people
Twenty health adult people were recruited for this study. All subjects were firstly subjected to routine medical examination and oral glucose tolerance test. After screen, nine voluntary men at 23-26 years of age (24.3±1.0) and seven women in 24-26 years of age (24.6±1.0) took the study. They were randomized into three groups (three men and two-three women per group) and tested simultaneously. They consumed one of the 40g glucose, 40g carbohydrate of RS rice (genetically modified rice) and WT rice (nongenetically modified rice) meal in 300 mL water with a washout period of 7-day. The WT and RS rice were cooked for rice meal. One week later, they were administrated with the second type of food and after another week, they were provided with the third type of food. Individual subjects arrived at the study site at 6 am. After resting for 30 min, individual was inserted with a catheter into the antecubital vein by a registered nurse. Their blood samples were collected and hydrogen breath was tested as the baseline values. At 7am, those subjects consumed individual food within 10 min. Their blood samples (2 mL) were collected at 0, 15, 30, 45, 60, 90, 120, 180, and 240 min post food intake and simultaneously subjected to hydrogen breath tests for indicated time points. The collected blood samples in grey-top BD Vacutainer blood tubes (special for blood glucose test) were centrifuged at 3000 g for 15 min at room temperature. The plasma was collected and stored at -20℃for less than 3 days for analysis, which did not significantly change the value of plasma glucose in our preliminary studies. Hydrogen breath testes for individual subjects were performed at 0 and 3.5-16h post food consumption with a half-hour interval between 3.5-14h and one-hour interval between 14-16h on a portable breath hydrogen analyzer. Subjects were provided special diner on the day before testing, lunch and dinner after the last blood collection (5h and 11h after the beginning of experiments) with little hydrogen-producing foods. The amount and kind of foods individuals consumed were recorded. The subjects were requested to consume equal amount of the same kind of foods at lunch and dinner when they participated in testing for the second and third type of foods.
Results
1. Subchronic toxicity test of the genetically modified rice with double antisense SBE gene
The weigh of rats and daily intake were not different among all the groups (P>0.05). At the middle of the experiment, MCV in female rats of GM group was higher than in those of No-GM group (P<0.05), Mo less than that in ND group (P<0.05), AST activity higher than that in ND group (P<0.05). ALT activity in female rats of Half-GM was higher than in those of ND and No-GM groups (P<0.05). Male rats of GM group had higher MCV than that in ND group (P<0.05). At the end of the experiment, MCH in female rats of GM group was higher than in those of No-GM group (P<0.05), AST and ALT activity higher than that in ND group (P<0.05). HCT and BUN level in male rats of GM group were less than in those of No-GM group (P<0.05), Mo level higher than that in ND group (P<0.05).
To female rats, brain index of GM group was higher than that in No-GM group and kidney index of ND group was higher than that in other groups(P<0.05). To male rats, all index had no significant difference among all the groups (P>0.05). Blood lipids, calcium and bone mineral density were also no significant difference(P>0.05). Among all the groups, no notable abnormity was found in the pathological examination on the main purtenances (P>0.05).
2. Effects of the genetically modified rice with double antisense SBE gene on the large bowel health in rats
Rats of GM group had similar body weight with ND group and significantly less than that of No-GM group (P<0.05). In comparison with No-GM and ND groups, fecal bulk and moisture, cecum weight and contents weigh in rats of GM and Half-GM groups had enhanced significantly(P<0.05). Colon weight in rats of GM group also were higher than in those of No-GM and ND groups (P<0.05). The concentration of short-chain fatty acid (SCFA) in the cecum, colon and fecal dropped gradually among all the groups. Compared with No-GM and ND groups, SCFA level of cecum and colon enhanced significantly in rats of GM and Half-GM groups (P<0.05) except colon butyric acid in rat of Half-GM group. In all groups, there were differences of acetic acid and propionic level in feces (P<0.05) but no difference of butyric acid. Cecal and fecal pH were lower in rats of GM and Half-GM groups than in those of other groups. (P<0.05).
3. The preventive effects of the genetically modified rice with double antisense SBE gene on high fat diet induced blood lipids abnormalities in rats
The initial weigh of rats and daily intake were not different among all the groups (P>0.05). At 4w, rats of NoGM-HF、GM-HF、HGM-HF and HF groups had higher weight than that of ND group (P<0.05), and the significant difference kept in the end. Compared with ND group, serum TG concentration in rats of other groups had no difference until termination. Serum TC contents in rats of NoGM-HF、GM-HF、HGM-HF and HF groups were significantly higher than in those of ND group from 4w to 13w, but there were not different among these groups (NoGM-HF、GM-HF、HGM-HF and HF) (P>0.05). Serum HDL-C contents were not different among all the groups (P>0.05), so as liver TG and TC concentration.
4. Study on the digestibility of important nutrients in the genetically modified rice with double antisense SBE gene in vivo
The apparent and true digestibility of all amino acids and crude protein had no significant difference in the two rices (P>0.05). The digestibility of carbohydrate and energy in genetically modified rice was significantly lower than that in nongenetically modified rice (P<0.05). The AAS value of genetically modified rice and nongenetically modified rice were 75% and 62%, corresponding PDCAAS value were 65% and 56%, respectively.
5. Postprandial glycemic and insulinemic responses to genetically modified rice with double antisense SBE gene and its fermentation in the large bowel of healthy people
The mean baseline blood glucose levels before the RS, WT rice, or glucose intake were similar (4.7±0.3 mmol/L vs 4.6±0.4 mmol/L vs 4.7±0.3 mmol/L, P>0.05), respectively. The value of plasma glucose for the RS rice meal was significantly smaller than that for the WT rice meal (P<0.05), particularly at 30, 45, 60, 90 and 120min post intake of meals. The highest levels of blood glucose after consuming RS rice (6.8±0.4 mmol/L) were significantly lower than that with WT rice (7.2±0.6 mmol/L, P<0.05). Importantly, the GI for the RS rice meal (48.4±21.8) was lower than of the WT rice meal (77.4±34.9, P<0.05).
The mean baseline insulin levels before the RS, WT rice, or glucose intake were similar (6.7±2.3μIU/mL vs 6.8±2.7μIU/mL vs 6.1±1.5μIU/mL, P>0.05), respectively. The levels of plasma insulin in subjects with the RS rice were significantly lower than that with WT rice at 45, 60, 90 and 120 min after food intake. After adjusting to the reference glucose (100%), the mean value of II in subjects with the RS rice meal (34.2±18.9) was significantly lower than that with the WT rice meal (54.4±22.4, P<0.05).
There was no significant difference in the baseline levels of fasting breath hydrogen before intake of RS and WT rice meal. In contrast, the levels of breath hydrogen after the RS rice were remarkably higher, as compared with that after the WT rice (P<0.05). The levels of hydrogen significantly increased 5 h after the RS rice, reached the highest level near 7 h and flatted until 14 h, followed by declining slightly. The peak levels of breath hydrogen after the RS rice meal (38.9±10.5ppm) were significantly higher than after the WT rice (17.6±3.7ppm, P<0.05).
Conclusions
1. Based on the results of the 90-day safety study in Wistar rats fed genetically modified rice with double antisense SBE gene, there were no enough evidences to confirm that the genetically modified rice had adverse effects on the rats.
2. Consumption of the genetically modified rice can improve large bowel health-related indexes and have active healthy effects on rat's large bowel.
3. Blood lipids abnormalities were successfully induced in the rats after feeding them high fat die. But consumption of the genetically modified rice had no preventive effect on the development of blood lipids abnormalities in rats.
4. The apparent and true digestibility of all amino acids and crude protein were not greatly changed by the increase of resistant starch content in the genetically modified rice. The digestibility of carbohydrate and energy in genetically modified rice was significantly lower than that in nongenetically modified rice owing to its resistant starch, which kept its character that are not absorbed in the small intestine. The AAS and PDCAAS value of genetically modified rice were higher than that of the nongenetically modified rice, so the two rices have substantial equivalence in the nutrition and feeding value of amino acid.
5. Consumption of the genetically modified rice meal decreased the postprandial glycemic and insulinemic responses and promoted resistant starch fermentation -related production of hydrogen in the large bowel of young and healthy Chinese adults.
引文
1.Englyst H N,Cummings J H.Digestion of the polysaccharides of some Cereal foods in the human small intestine.Clin Nutr,1985,42:778-787.
2.Englyst HN,Kingman SM,Cummings JH.Classification and measurement of nutritionally important starch fractions.Eur J Clin Nutr,1992,46:S33-S50.
3.Brown IL,Mcnaught KJ,Moloney E.Hi-maize~(TM):new directions in starch technology and nutrition.Food Aust,1995,47:272-275.
4.张文青,张月明,杨月欣.抗性淀粉-功能性食物成分.国外医学卫生学册,2005,32:232-235.
5.郭春锋,李婧妍,张守文.抗性淀粉生理功能研究进展.食品科技,2006:1-3.
6.杨朝柱,李春寿,舒小丽等.富含抗性淀粉水稻突变体的淀粉特性.中国水稻科学,2005,19:516-520.
7.阮少兰,刘亚伟,阮竟兰.大米抗性淀粉制备工艺研究.粮食与饲料工业,2005.7:16-17.
8.徐丹鸿,徐红华.抗性淀粉制备及其性质研究.粮食与油脂,2005,4:9-11.
9.Parchure AA,Kulkarni PR.Effect of food processing treatments on generation of resistant starch.Int J Food Sci Nutr,1997,48:257-260.
10.Herman K,Song Y,Jay-lin J.Effect and mechanism of ultrahigh hydrostatic pressure on the structure and properties of starched.Carbohyd Polym,2002,47:233-244.
11.焦桂爱,唐绍清,罗炬.水稻抗性淀粉突变体抗性淀粉结构的比较研究.中国水稻科学,2006,20:645-648.
12.Cummings JH,Macfarlane GT.The control and consequences of bacterial fermentation in the human large intestine.J Appl Bacteriol,1991,70:443-459.
13.Ahmad MS,Krishnan S,Ramakrishna BS,et al.Butyrate and glucose metabolism by colonocytes in experimental colitis in mice.Gut,2000,46:493-499.
14.Bauer MM,Florian S,Muller SK,et al.Dietary resistant starch type 3 prevents tumor induction by 1,2-dimethylhydrazine and alters proliferation,apoptosis and dedifferentiation in rat colon.Carcinogenesis,2006,27:1849-1859.
15.Vemia P,Annese V,Bresci G,et al.Topical butyrate improves efficacy of 5-ASA in refractory distal ulcerative colitis:results of a multicentre trial.Eur J Clin Invest,2003,33:244-248.
16.Behall KM,Hallfrisch JG,Scholfield DJ,et al.Consumption of both resistant starch and beta-glucan improves postprandial plasma glucose and insulin in women.Diabetes Care,2006,29:976-981.
17.Park OJ,Kang NE,Chang MJ,et al.Resistant starch supplementation influences blood lipid concentrations and glucose control in overweight subjects.J Nutr Sci Vitaminol,2004,50:93-99.
18.王竹,杨月欣,韩军花等.抗性淀粉对饮食诱发葡萄糖耐量异常的预防.营养学报,2002,24:48-51.
19.王红伟,韩军花,张文青等.抗性淀粉对大鼠胰岛素抵抗的影响.营养学报,2007,29:131-134.
20.Behall KM,Scholfield DJ,Hhallfrisch JG.Barley beta-glucan reduces plasma glucose and insulin responses compared with resistant starch in men.Nutr Res,2006,26:644-650.
21.Han KH,Fukushima M,Kato T,et al.Enzyme-resistant fractions of beans lower serum cholesterol and increased sterol excretions and hepatic mRNA levels in rats.Lipid,2003,38:919-924.
22.Lopez HW,Levrat-Verny MA,Coudray C,et al.Class 2 resistant starches lower plasma and liver lipids and improve mineral retention in rats.J Nutr,2001,131:1283-1289.
23.Younes H,Levrat MA,Demigne C,Remesy C.Resistant starch is more effective than cholestyramine as a lipid-lowering agent in the rat.Lipids,1995,30:847-853.
24.Vanhoof K,De Schrijver R.Consumption of enzyme resistant starch and cholesterol metabolism in normo-and hypercholesterlemic rats.Nutr Res,1997,17:1331-1340.
25.Kim WK,Chung MK,Kang NE,et al.Effect of resistant starch from corn or rice on glucose control,colonic events,and blood lipid concentrations in streptozotocin-induced diabetic rats.J Nutr Biochem,2003,14:166-172.
26.Cheng HH,Lai MH.Fermentation of resistant rice starch produces propionate reducing serum and hepatic cholesterol in rats.J Nutr,2000,130:1991-1995.
27.张文青,张月明,朱虎虎.抗性淀粉对大鼠肝脏胆固醇代谢相基因表达的 影响.营养学报,2007,29(5):458-462.
28.葛可佑.中国营养科学全书[M].人民卫生出版社,2004.
29.Reves PG,Nielsen FH,Fahey GC.AIN-93 Purified diets for laboratory rodents:final report of the American Institute of Nutrition Ad Hoc writing committee on the reformulation of the AIN-76A rodent diet.J Nutr,1993,123:1939-1951.
30.Momma K,Hashimoto W,Yoon HJ,et al.Safety assessment of rice genetically modified with soybean glycinin by feeding studies on rats.Biosci Biotechnol Biochem,2000,64:1881-1886.
31.Hashimoto W,Momma K,Yoon HJ,et al.Safety assessment of transgenic potatoes with soybean glycinin by feeding studies in rats.Biosci Biotechnol Biochem,1999,63:1942-1946.
32.Baghurst PA,Baghurst KI,Record SJ.Dietary fibre,non-starch polysaccharides and resistant starch:a review.Food Aust,1996,48:S3-S35.
33.Brighenti F,Casiraqhi MC,Baqqio C.Resistant starch in the Italian diet.Br J Nutr,1998,80:333-341.
34.Murphy MM,Douglass JS,Birkett A.Resistant starch intakes in the United States.J Am Diet Assoc,2008,108:67-78.
35.Schroder M,Poulsen M,Wilck A,et al.A 90-day safety study of genetically modified rice expressing CrylAb protein(Bacillus thuringiensis toxin) in Wistar rats.Food Chem Toxicol,2007,45:339-349.
36.Poulsen M,Kroghsbo S,Schroder M.A 90-day safety study in Wistar rats fed genetically modified rice expressing snowdrop lectin Galanthus nivalis(GNA).Food Chem Toxicol,2007,45:350-363.
37.詹纯列,肖育华,李新春等.普通级、SPF级SD、Wistar大鼠血液生化常值的测定与比较.中国比较医学杂志,2004,14:94-96.
38.张敏,纪晓光,王京燕.清洁级Wistar大鼠血常规及生化指标正常值观察.中国消毒学杂志,2006,23:119-123.
39.詹纯列,肖育华,王露霞等.普通级、SPF级SD大鼠、Wistar大鼠血常规的测定与比较.广东医学,2002,23:1025-1026.
40.尚晓娅,高群玉,王捷等.抗性淀粉食品安全性毒理学研究.毒理学杂志,2006,20:310-311.
41.严梅荣,王丹丹.抗性淀粉产品的安全性及其食品标签.粮食与饲料工业, 2006,3:22-23.
42. Hill MJ. Bacterial fermentation of complex carbohydrates in the human colon. Eur J Cancer Prev, 1995, 4:353-358.
43. Pickard KM, Bremner AR, Gordon JN, et al. Microbial-gut interactions in health and disease. Immune responses. Best Pract Res Clin Gastroenterol, 2004, 18: 271-285.
44. Koruda MJ, Rolandelli RH, Bliss DZ, et al. Parenteral nutrition supplemented with short-chain fatty acid: effect on the small bowel mucosa in normal rats. Am J Clin Nutr, 1990, 51:685-689.
45. Gibson GR, Roberfroid MB. Dietary modulation of the human colonic microbiota: introducing the concept of prebiotics. J Nutr, 1995, 125:1401-1412.
46. Phillips J, Muir JG, Birkett A, et al. Effect of resistant starch on fecal bulk and fermentation-dependent event in humans. Am J Clin Nutr, 1995, 62:121-130.
47. Keenan MJ, Zhou J, McCutcheon KL, et al. Effects of resistant starch, a non-digestible fermentable fiber, on reducing body fat. Obesity (Silver Spring), 2006, 14:1523-1534.
48. Higgins JA, Brown MA, Storlien LH. Consumption of resistant starch decreases postprandial lipogenesis in white adipose tissue of the rat. J Nutr, 2006, 5:25.
49. Levrat MA, Moundras C, Younes H, et al. Effectiveness of resistant starch, compared to guar gum, in depressing plasma cholesterol and enhancing fecal steroid excretion. Lipids, 1996, 31:1069-1075.
50. Thornton JR. High colonic pH promotes colorectal cancer. Lancet, 1981, 1:1081-1083.
51. Walker AR, Walker BF, Walker AJ. Fecal pH, dietary fiber intake, and proneness to colon cancer in four South African populations. Br J Cancer, 1986, 53:489-495.
52. Malhotra SL. Fecal urobilinogen levels and pH of stools in population groups with different incidence of cancer of the colon, and their possible role in its aetiology. J R Soc Med, 1982, 75:709-714.
53. Sellin JH, DeSoignie R, Burlingame S. Segmental differences in short-chain fatty acids transport in rabbit colon: effect of pH and Na. J Membr Biol, 1993, 136:147-158.
54. Walker AW, Duncan SH, McWilliam Leitch EC, et al. pH and peptide supply can radically alter bacterial populations and short-Chain fatty acid ratios within microbial communities from the human colon. Appl Environ Microbiol, 2005, 71:3692-3700.
55. Van Munster IP, Tanqerman A, Naqenqast FM. Effect of resistant starch on colonic fermentation, bile acid metabolism and mucosal proliferation. Dig Dis Sci, 1994, 39:834-842.
56. Noakes M, Clifton PM, Nestel PJ, et al. Effect of high amylose starch and oat bran on metabolic variables and bowel function in subjects with hypertriglyceridemia. Am J Clin Nutr, 1996, 64: 944-951.
57. Cummings JH, Beatty ER, Kingman SM, et al. Digestion and physical properties of resistant starch in the human large bowel. Br J Nutr, 1996, 75:733-747.
58. Ruppin H, Bar-Meir S, Soergel KH. Absorption of short-chain fatty acids by the colon. Gastroenterology, 1980, 78:1500-1507.
59. Roediger WE. Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man.Gut, 1980, 21:793-798.
60. Annison G, Illman RJ, Topping DL. Acetylated, propionylated or butyrylated starches raise large bowel short-chain fatty acids preferentially when fed to rats. J Nutr, 2003,133:3523-3528.
61. Macfarlane GT, Gibson GR, Cummings JH. Comparison of fermentation reactions in different regions of the human colon. J Appl Bacteriol, 1992, 72:57-64.
62. Beaulieu KE, Mcburne MI. Changes in pig serum lipids, nutrient digestibility and sterol excretion during cecal infusion of propionate. J Nutr, 1992, 122:241-245.
63. Han KH, Fukushima M, Schimizu K, et al. Resistant starches of beans reduce the serum cholesterol concentration in rats. J Nutr Sci Vitaminol, 2003, 49:281-286.
64. Han KH, Sekikawa M, Shimada K, et al. Resistant starch fraction prepared from kintoki bean affects gene expression of genes associated with cholesterol metabolism in rats. Exp Biol Med, 2004, 229:787-792.
65. Figurska CD, Orzel D, Styczynska M, et al. The influence of RS4 resistant starch on wistar rats metabolism. Biochemical and lipid indices. Rocz Panstw Zakl Hig,2007,58:1-6.
66.De Deckere EA,Kloots W J,van Amelsvoort JM.Resistant starch decreases serums total cholesterol and triacylglycerol concentration in rats.J Nutr,1993,123:2142-2151.
67.Fernandez ML,Roy S,Vergara Jimenez,M.Resistant starch and cholestyramine have distinct effects on hepatic cholesterol metabolism in guinea pigs fed a hypercholesterolemic diet.Nutr Res,2000,20:837-849.
68.Han KH,Iijuka M,Shimada K,et al.Adzuki resistant starch lowered serum cholesterol and hepatic 3-hydroxy-3-methylglutaryl-CoA mRNA levels and increased hepatic LDL-receptor and cholesterol 7a-hydroxylase mRNA levels in rats fed a cholesterol diet.Br J Nutr,2005,94:902-908.
69.Jenkins DJ,Vuksan V,Kendall CW,et al.Physiological effects of resistant starches on fecal bulk,short chain fatty acids,blood lipids and glycemic index.J Am Coll Nutr,1998,17:609-616.
70.霍启光.饲料生物学评定技术[M].中国农业出版社,1996.
71.Fastinger ND,Mahan DC.Effect of soybean meal particle size on amino acid and energy digestibility in grower-finisher swine.J Anim Sci,2003,81:697-704.
72.Han JH,Yang YX,Men JH,et al.Comparison of ileal digested production of parental rice and rice genetically modified with cowpeas trypsin inhibitor.Biomed Environ Sci,2006,19:42-46.
73.Nyachoti CM,De Lange CF,Schulze H.Estimating endogenous amino acid flows at the terminal ileum and true ileal amino acid digestibilites in feedstuffs for growing pigs using the homoarginine method.J Anim Sci,1997,75:3206-3213.
74.Libao-Mercado AJ,Yin Y,Van Eys J,De Lange CF.True ileal amino acid digestibility and endogenous ileal amino acid losses in growing pigs fed wheat shorts- or casein-based diets.J Anim Sci,2006,84:1351-1361.
75.杨月欣.中国食物成分表[M].北京大学医学出版社,2002.
76.Smiricky MR,Grieshop CM,Albin DM,et al.The influence of soy oligosaccharides on apparent and true ileal amino acid digestibilities and fecal consistency in growing pigs.J Anim Sci,2002,80:2433-2441.
77.靳洪涛,凡春荣,李慧,等.实验用五指山小型猪正常生理值测定.实验动 物,2007,24:69-73.
78.谢忠忱,黄广勇,陈华,等.五指山小型猪高脂血症模型的建立.中国比较医学杂志,2006,16:537-540.
79.Protein quality evalution.Report of a joint FAO/WHO expert consultation[M].Bethesda,USA,1989.
80.Butts CA,Moughan P J,Smith WC,et al.Endogenous lysine and other amino acid flows at the terminal ileum of the growing pigs(20kgbody weight):the effect of protein-free,synthetic amino acid,peptide and protein alimentation.J Sci Food Agri,1993,61:31-40.
81.Donkoh A,Moughan PJ.Endogenous ileal nitrogen and amino acid flows in the growing pig receiving a protein-free diet and diets containing enzymically hydrolysed casein or graded levels of meat and bone meal.J Anim Sci,1999,68:511-518.
82.吴群,熊平,陈实,等.近交系海南五指山猪SLA经典Ⅰ类和Ⅱ类分子序列分析.现代免疫学,2004,24:23-26.
83.Jenkins DJ,Wolever TM,Taylor RH,et al.Glycemic index of foods:a physiological basis for carbohydrate exchange.Am J Clin Nutr,1981,34:362-366.
84.Mckeown NM,Meigs JB,Liu S,et al.Carbohydrate nutrition,insulin resistance,and the prevalence of the metabolic syndrome in the Framingham offspring cohort.Diabetes Care,2004,27:538-546.
85.Higgins JA,Brand Miller JC,Denyer GS.Development of insulin resistance in the rat is dependent on the rate of glucose absorption from the diet.J Nutr,1996,126:596-602.
86.Jenkins DJ,Kendall CW,Augustin LS,et al.Glycemic index:overview of implications in health and disease.Am J Clin Nutr,2002,76:266S-273S.
87.Musch MW,Bookstein C,Xie Y,et al.SCFA increase intestinal Na absorption by induction of NHE3 in rat colon and human intestinal C2/bbe cells.Am J Physiol Gastrointest Liver Physiol,2001,280:G687-G693.
88.Vernia P,Annese V,Bresci G,et al.Topical butyrate improves efficacy of 5-ASA in refractory distal ulcerative colitis:results of a multicentre trial.Eur J Clin Invest,2003,33:244-248.
89.Luhrs H,Gerke T,Schauber J,et al.Cytokine-activated degradation of inhibitory kappaB protein alpha is inhibited by the short chain fatty acid butyrate. Int J Colorect Dis, 2001, 16:195-201.
90. Dashwood RH, Myzak MC, Ho E. Dietary HDAC inhibitors: time to rethink weak ligands in cancer chemoprevention?. Carcinogenesis, 2006, 27:344-349.
91. Mortensen PB, Clausen MR. Short-chain fatty acids in the human colon:relation to gastrointestinal health and disease. Scand J Gastroenterol Suppl, 1996,216:132-148.
92. Wolever TM, David JA, Alexandra LJ. The glycemic index: methodology and clinical implication. Am J Clin Nutr, 1991, 54:846-854.
93. Symonds EL, Kritas S, Omari TI, Butler RN. A combined 13CO2/H2 breath test can be used to assess starch digestion and fermentation in humans. J Nutr, 2004,134:1193-1196.
94. Wolever TM. Carbohydrate and the regulation of blood glucose and metabolism. Nutr Rev, 2003, 61:S40-S48.
95. Bornet FR, Costagliola D, Rizkalla SW, et al. Insulinemic and glycemic indexes of six starch-rich foods taken alone and in a mixed meal by type 2 diabetics. Am J Clin Nutr, 1987, 45:588-95.
96. Behall KM, Hallfrisch J. Plasma glucose and insulin reduction after breads varying in amylose content. Eur J Clin Nutr, 2002, 56:913-920.
97. Granfeldt Y, Drews A, Bjorck I. Arepas made from high amylose corn flour produce favorably low glucose and insulin response in healthy humans. J Nutr, 1995, 125:459-465.
98. Hatonen KA, Simila ME, Virtamo JR, et al. Methodologic considerations in the measurement of glycemic index: glycemic response to rye bread, oatmeal porridge, and mashed potato. Am J Clin Nutr, 2006, 84:1055-1061.
99. Wolever T. Comment on the validity of glycaemic glucose equivalent. Euro J Clin Nutr, 2004, 58:1672-1673.
100. Levitt MD. Production and excretion of hydrogen gas in man. N Engl J Med, 1969,281:122-127.
101. Cummings JH. The Large Intestine in Nutrition and Disease[M]. Brussels Institute Danone, 1997.
102. Asp ML, Hertzler SR, Chow J, Wolf BW. Gamma-cyclodextrin lowers postprandial glycemia and insulinemia without carbohydrate malabsorption in healthy adults. J Am Coll Nutr, 2006, 25:49-55.
1.ENGLYST H N,KINGMAN S M,CUMMINGS J H.Classification and measurement of nutritionally important starch fractions[J].Eur J Clin Nutr,1992,46(2):S33-S50.
2.HEDEMANN M S,KNUDSEN K E.Resistant starch for weaning pigs-Effect on concentration of short chain fatty acids in digesta and intestinal morphology[J].Livestock Science,2007,108(1):175-177.
3.AHMAD M S,KRISHNAN S,RAMAKRISHNA B S,et al.Butyrate and glucose metabolism by colonocytes in experimental colitis in mice[J].Gut,2000,46(4):493-499.
4.BAUER M M,FLORIAN S,MULLER S K,et al.Dietary resistant starch type 3prevents tumor induction by 1,2-dimethylhydrazine and alters proliferation,apoptosis and dedifferentiation in rat colon[J].Carcinogenesis,2006,27(9):1849-1859.
5.MAI A,MASSA S,ROTILI D,et al.Histone deacetylation in epigenetics:an attractive target for anticancer therapy[J].Med Res Rev,2005,25(3):261-309.
6.DASHWOOD R H,MYZAK M C,Ho E.Dietary HDAC inhibitors:time to rethink weak ligands in cancer chemoprevention?[J]. Carcinogenesis,2006,27(2):344-349.
7. DAVIE J R. Inhibition of histone deacetylase activity by butyrate[J]. J Nutr,2003,133(7):2485S-2493S.
8. VAN DER S M, DE KONING B A, DE BRUIJN A C, et al. Muc2-deficient mice spontaneously develop colitis, indicating that Muc2 is critical for colonic protection[J]. Gastroenterology,2006,131(1):117-129.
9. HATAYAMA H, IWASHITA J, KUWAJIMA A, et al. The short chain fatty acid, butyrate, stimulates MUC2 mucin production in the human colon cancer cell line, LS174T[J]. Biochem Biophys Res Commun,2007,356(3):599-603.
10. TODEN S, BIRD A R, TOPPING D L, et al. Resistant starch prevents colonic DNA damage induced by high dietary cooked red meat or casein in rats[J]. Cancer Biol Ther, 2006,5(3):267-272.
11. SUZUKI T, YOSHIDA S, HARA H. Physiological concentrations of short-chain fatty acids immediately suppress colonic epithelial permeability[J]. Br J Nutr,2008,100(2):297-305.
12. VEMIA P, ANNESE V, BRESCI G, et al. Topical butyrate improves efficacy of 5-ASA in refractory distal ulcerative colitis: results of a multicentre trial[J]. Eur J Clin Invest,2003,33(3): 244-248.
13. LUHRS H, GERKE T, SCHAUBER J, et al. Cytokine-activated degradation of inhibitory kappaB protein alpha is inhibited by the short chain fatty acid butyrate[J]. Int J Colorect Dis,2001,16(4): 195-201.
14. MUSCH MW, BOOKSTEIN C, XIE Y, et al. SCFA increase intestinal Na absorption by induction of NHE3 in rat colon and human intestinal C2/bbe cells[J]. Am J Physiol Gastrointest Liver Physiol,2001,280(4):G687-G693.
15．何梅,洪洁,杨月欣等．抗性淀粉对大鼠肠道菌群的影响[J]．卫生研究,2005,34(1)：85-87．
16. RIDLON J M, HYLEMON P B. A potential role for resistant starch fermentation in modulating colonic bacterial metabolism and colon cancer risk[J]. Cancer Biol Ther,2006,5(3):273-274.
17. MCKEOWN N M, MEIGS J B, LIU S, et al. Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham offspring cohort[J]. Diabetes Care,2004,27(2):538-546.
18. BEHALL K M, HALLFRISCH J G, SCHOLFIELD D J, et al. Consumption of both resistant starch and beta-glucan improves postprandial plasma glucose and insulin in women[J].Diabetes Care,2006,29(5):976-981.
19.PARK O J,KANG N E,CHANG M J,et al.Resistant starch supplementation influences blood lipid concentrations and glucose control in overweight subjects[J].J Nutr Sci Vitaminol,2004,50(2):93-99.
20.王竹,杨月欣,韩军花等.抗性淀粉对饮食诱发葡萄糖耐量异常的预防[J].营养学报,2002,24(1):48-51.
21.王红伟,韩军花,张文青等.抗性淀粉对大鼠胰岛素抵抗的影响[J].营养学报,2007,29(2):131-134.
22.KIM W K,CHUNG M K,KANG N E,et al.Effect of resistant starch from com or rice on glucose control,colonic events,and blood lipid concentrations in streptozotocin-induced diabetic rats[J].J Nutr Biochem,2003,14(3):166-172.
23.BEHALL K M,SCHOLFIELD D J,HALLFRISCH J G.Barley beta-glucan reduces plasma glucose and insulin responses compared with resistant starch in men[J].Nutr Res,2006,26(12):644-650.
24.HAN K H,FUKUSHIMA M,KATO T,et al.Enzyme-resistant fractions of beans lower serum cholesterol and increased sterol excretions and hepatic mRNA levels in rats[J].Lipid,
25.2003,38(9):919-924.
26.LOPEZ H W,LEVRAT-VERNY M A,COUDRAY C,et al.Class 2 resistant starches lower plasma and liver lipids and improve mineral retention in rats[J].J Nutr,2001,131(4):1283-1289.
27.CHENG H H,LAI M H.Fermentation of resistant rice starch produces propionate reducing serum and hepatic cholesterol in rats[J].J Nutr,2000,130(8):1991-1995.
28.BEAULIEU K E,MCBURNEY M I.Changes in pig serum lipids,nutrient digestibility and sterol excretion during cecal infusion of propionate[J].J Nutr,1992,122(2):241-245.
29.张文青,张月明,朱虎虎.抗性淀粉对大鼠肝脏胆固醇代谢相基因表达的影响[J].营养学报,2007,29(5):458-462.
30.FIGURSKA C D,ORZEL D,STYCZYNSKA M,et al.The influence of RS4resistant starch on wistar rats metabolism.Biochemical and lipid indices[J].Rocz Panstw Zakl Hig,2007,58(1):1-6.
31.徐丹鸿,徐红华.抗性淀粉制备及其性质研究[J].粮食与油脂,2005,4:9-11.
32.苏宁,万向元,翟虎渠等.功能型水稻研究现状和发展趋向[J].中国农业科学,2007,40(3):433-439.
33.陈光,高俊鹏,王刚等.抗性淀粉的功能特性及应用研究现状[J].吉林农业大学学报,2005,27(5):578-581.