胰岛素和酶解配方乳对初生仔猪胃肠道生长发育影响的研究

为研究胰岛素和酶解配方乳是否促进初生仔猪胃肠道的生长发育 ,本试验比较了饲喂配方乳、配方乳补加胰岛素(60mIU/ml)或酶解(胰蛋白酶和糜蛋白酶)配方乳3天后仔猪胃肠的重量 ,肠道长度 ,肠粘膜DNA、RNA和蛋白质含量 ,血浆中皮质醇、胰岛素和胃泌素的水平。饲喂配方乳补加胰岛素或酶解配方乳的仔猪与饲喂配方乳的仔猪相比 ,胃、小肠、结肠的重量 ,小肠和结肠的长度 ,小肠粘膜DNA、RNA含量和结肠粘膜DNA、RNA、蛋白质含量均无显著变化(P>0.05) ;血浆中皮质醇、胰岛素水平也无显著差异(P>0.05)。但饲喂配方乳补加胰岛素的仔猪小肠粘膜尤其是回肠后段粘膜的重量(P<0.05)和蛋白质含量(P<0.01)显著高于饲喂配方乳的仔猪 ;饲喂酶解配方乳仔猪血浆的胃泌素水平均显著(P<0.01)高于饲喂配方乳的仔猪 ,酶解配方乳中可能含有刺激初生仔猪胃泌素释放的物质     

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１中俄猪１６个遗传标记基因位点的多态性与繁殖性状的相关研究２大白猪繁殖和生产性状母体遗传效应估计３奶牛泌乳曲线的拟合及其模型参数的遗传分析４胰岛素和酶解配方奶粉对初生仔猪小肠生长发育的影响５日粮铜水平对肉仔鸡生长性能和免疫功能影响的研究６饲粮完整蛋白...     

酪蛋白酶解物在断奶应激中对仔猪小肠性能维护试验

为探讨酪蛋白酶解物中活性肽在断奶应激中对小肠性能的维护,在pH为1.4、37℃.隋况下,将酪蛋白经胃蛋白酶消化2小时,酶解物用于对比试验。将20头21日龄断乳仔猪随机分成试验组和对照组,试验组每头每天饲喂20ml酶解物,对照组只饲喂基础日粮。结果表明,饲喂酶解物的仔猪小肠受应激影响小,1周后比对照组绒毛高出26.66%(P<0.01),隐窝低出15.75％(P<0.05);大肠杆菌减少17.21％(P<0.01),乳酸杆菌、双歧杆菌分别增加了6.49％、6.87％(P<0.01)。     

仔猪人工乳的配制和饲喂方法

有些母猪产仔后泌乳不足或无乳,仔猪需配制人工乳饲喂,才能使其发育生长良好,提高仔猪成活率和育成率。有些人单纯用鲜牛奶或奶粉冲开水饲喂,但仍不能满足仔猪对各种营养物质特别是各种微量元素的需要,而且成本昂贵,经济效益差。现介绍几种仔猪人工乳的配方、制法及饲喂方法。有鲜牛奶或奶粉作基础的人工乳配     

膨化与加酶玉米对断奶仔猪血液指标及胰腺和肠道淀粉酶活性的影响

选择96头断奶仔猪，随机分为4组，每组6个重复，每个重复4头仔猪，分别饲喂普通玉米、膨化玉米、普通玉米加酶及膨化玉米加酶为主要能量原料的饲料，研究了膨化与加酶玉米对断奶仔猪血液指标以及胰腺组织和小肠内容物淀粉酶活性的影响。结果表明，膨化和加酶处理玉米以及二者互作对断奶仔猪血清葡萄糖和尿素氮浓度均无显著影响。膨化和加酶处理均可显著提高仔猪断奶14d时十二指肠和空肠内容物的淀粉酶活力。对断奶28d时胰腺和小肠各段内容物淀粉酶活性均无影响；在整个试验期，未见到膨化和加酶处理的互作。     

速溶酶解发酵乳化饲料对断奶仔猪生产性能、养分消化率和肠道菌群的影响

选取400头23日龄健康的"杜×长×大"三元杂交断奶仔猪,随机分为5组,每组8个重复,每个重复10头仔猪.对照组不添加速溶酶解发酵乳化饲料,对照组饲喂基础日粮,试验一组饲喂基础日粮+4.0％速溶酶解发酵乳化饲料,试验二组饲喂基础日粮+6.0％速溶酶解发酵乳化饲料,试验三组饲喂基础日粮+8.0％速溶酶解发酵乳化饲料,试验...     

释放仔猪生长潜力的试验报告

仔猪具有较大的生长潜力,而母乳及乳猪饲料均未完全将其生长潜力释放出来.本试验采用仔猪奶粉对断奶前与断奶后的仔猪进行补充饲喂,即断奶前采用"母乳 仔猪专用奶粉 乳猪饲料"、断奶后采用"仔猪专用奶粉 乳猪饲料"的饲喂模式,可以明显地提高哺乳仔猪和断乳仔猪的增重,并对其后期增重有延续性的促进作用.     

豆粕酶解发酵物对仔猪生长性能及部分营养物质粪排放量的影响

选择240头18 kg左右杜长大三元仔猪,随机分为2组,分别饲喂豆粕酶解发酵物10%替代豆粕的日粮和对照组日粮,以期研究不同的豆粕酶解发酵物对仔猪生长性能及部分营养物质粪排放量的影响。结果表明,饲喂豆粕酶解发酵物的仔猪平均日增重(ADG)和对照组相比显著提高了10.58%(P0.05),平均日采食量(ADI)比对照组显著提高了8.52%(P0.05)。粪中部分营养物质排放量方面饲喂豆粕酶解发酵物的仔猪粪中氮的排放量显著下降了8.22%(P0.05),磷、铜、锌的排放量有降低的趋势,但是差异不显著(P0.05)。结论,豆粕酶解发酵物对仔猪具有较好的促生长、降低排放的作用,可以作为仔猪良好植物性蛋白质饲料原料应用。     

胎儿宫内发育迟缓对新生仔猪小肠组织发育的影响

为研究胎儿宫内发育迟缓(IUGR)对新生仔猪肠道生长发育的影响,比较了初生组(D0)、母乳饲喂3 d组(D3)和母乳饲喂7 d组(D7)3组中正常仔猪和宫内发育迟缓仔猪的小肠长度和重量、组织形态学结构及黏膜DNA、RNA和蛋白质含量。结果显示,初生时,新生正常仔猪小肠总重和黏膜重、RNA和蛋白质含量显著高于IUGR仔猪(P<0.05)。新生IUGR仔猪小肠的肠壁厚度、绒毛高度显著低于正常仔猪(P<0.05);而IUGR仔猪相对于体重的小肠长度极显著高于正常仔猪(P<0.01)。生长至3日龄时,正常猪小肠长度、小肠黏膜重显著高于IUGR猪(P<0.05),小肠总重、肌肉重极显著高于IUGR猪(P<0.01);IUGR仔猪小肠的肠壁厚度、绒毛高度显著低于正常仔猪(P<0.05),而IUGR仔猪相对于体重的小肠长度显著高于正常仔猪(P<0.05)。7日龄时,正常猪的小肠黏膜RNA含量显著高于IUGR猪(P<0.05),其余指标没有显著差别。整个试验结果表明宫内发育迟缓对仔猪小肠组织发育造成不利影响,导致新生仔猪小肠黏膜重量、蛋白质含量、肠壁厚度和绒毛高度的降低;IUGR仔猪的小肠组织生长在出生后1周内能部分实现补偿,而且补偿生长的实现是随着日龄增加逐步完全的。     

嗜酸乳杆菌培养物对断奶仔猪肠道发育及消化酶活性的影响

研究旨在探讨在断奶仔猪饲粮中添加发酵豆粕及嗜酸乳杆菌培养物对仔猪肠道形态结构及空肠消化酶活性的影响。选用遗传背景、胎次和体重相近的21日龄断奶仔猪48头,随机分为4个处理,每个处理3个重复,每个重复4头仔猪。对照组仔猪饲喂玉米-豆粕型基础饲粮,试验Ⅰ组仔猪饲喂奶粉饲粮(由某公司提供),试验Ⅱ组仔猪饲喂用发酵豆粕代替10.0%普通豆粕的试验饲粮,试验Ⅲ组饲粮是在试验Ⅱ组基础上用嗜酸乳杆菌培养物代替3.0%原有原料,试验期21 d。结果显示:1饲粮中用发酵豆粕代替10%普通豆粕显著提高35日龄仔猪十二指肠、回肠绒毛高度,降低35日龄仔猪隐窝深度,提高绒毛高度/隐窝深度(V/C)(P0.05)。2饲粮添加3%嗜酸乳杆菌培养物显著提高了35日龄仔猪各段小肠的绒毛高度,降低35日龄仔猪各段小肠隐窝深度,提高42日龄各段小肠绒毛高度/隐窝深度(P0.05)。3通过透射电镜发现,对照组空肠微绒毛稀疏、短小、排列不整齐;试验组仔猪空肠微绒毛较长、整齐、密集,尤其是添加嗜酸乳杆菌组效果最好。4饲粮中用发酵豆粕代替10%普通豆粕显著提高了35日龄仔猪空肠蔗糖酶、麦芽糖酶活性(P0.05),提高42日龄仔猪麦芽糖酶活性(P0.05),提高42日龄仔猪麦芽糖酶活性。5饲粮添加3%嗜酸乳杆菌培养物与只添加发酵豆粕相比,仔猪空肠二糖酶、Ca2+/Mg2+-ATP酶活性差异不显著(P0.05),但35日龄时Na+/K+-ATP酶活性显著提高(P0.05)。发酵豆粕可改善仔猪空肠微绒毛结构,减缓断奶应激引起的乳糖酶急剧下降,提高蔗糖酶、麦芽糖酶活性。用嗜酸乳杆菌培养物替代原有原料3%后各指标效果更好,替代后其效果与奶粉饲粮的效果相当。     

胎儿宫内发育迟缓对新生仔猪小肠消化酶发育的影响

利用自然选择法从14窝初生仔猪选择14头正常仔猪和14头宫内发育迟缓（IUGR）仔猪，随机分成3组：初生组（DO）、母乳饲喂3d组（D3）和母乳饲喂7d组（D7），分别在0、3、7d屠宰以研究胎儿宫内发育迟缓对新生仔猪小肠消化酶发育的影响。初生时，正常仔猪小肠乳糖酶的总活性和比活性都显著高于IUGR仔猪。IUGR仔猪小肠氨基肽酶的总活性和比活性都低于正常仔猪，其中总活性的差异极显著。IUGR仔猪小肠的麦芽糖酶总活性显著低于正常仔猪，但比活性在2组间没有显著差异。2组间碱性磷酸酶的比活性和总活性都没有显著差异。生长至3日龄时，正常仔猪和IUGR仔猪间麦芽糖酶和碱性磷酸酶活性没有显著差异，而2组间乳糖酶总活性和氨基肽酶总活性的差异显著。7日龄时，正常仔猪和IUGR仔猪乳糖酶、麦芽糖酶、氨基肽酶和碱性磷酸酶活性均没有显著差异。试验结果表明宫内发育迟缓抑制了小肠乳糖酶和氨基肽酶的成熟，而麦芽糖酶和碱性磷酸酶表现出早熟。同时又表明，胎儿宫内发育迟缓仔猪的肠道功能发育在生后1周内能部分实现补偿生长，而且补偿生长的实现是随着日龄增加逐步完全的。     

Decreased activity of brush border membrane-bound digestive enzymes in small intestines from pigs experimentally infected with porcine epidemic diarrhea virus

Brush border membrane-bound digestive enzymes such as disaccharidases (lactase, sucrase, and maltase), leucine aminopeptidase N, and alkaline phosphatase were measured in jejunum from pigs experimentally infected with porcine epidemic diarrhea virus (PEDV). Three piglets from the infected and control groups were euthanized by electrocution and subjected to necropsy at 24, 36, 48, 60, and 72 hours post-inoculation (hpi). The infection of PEDV to jejunum resulted in significant decreases in brush border membrane-bound digestive enzymes such as disaccharidases (lactase, sucrase, and maltase), leucine aminopeptidase N, and alkaline phosphatase. PEDV replication results in massive destruction of villous enterocytes leading to a marked reduction of intestinal epithelial surface and brush border membrane-bound digestive enzyme activity. Reduced enzymatic activity and villous atrophy in the small intestine is thought to result in a maldigestive and malabsorptive diarrhea.     

Influence of dietary forage and feed intake on carbohydrase activities and small intestinal morphology of calves.

Twenty (12 Holstein, 8 Longhorn cross) calves (198 kg and 7 mo old) were used in a randomized complete block design to evaluate the effects of dietary forage concentration and feed intake on carbohydrase activities and small intestinal (SI) morphology. Calves were individually fed 90% forage (alfalfa) or a 90% concentrate (50% sorghum: 50% wheat) diet at either one or two times NEm for 140 d and slaughtered; tissues and small intestinal digesta were collected. Increased feed intake increased (P less than .05) pancreatic weight, alpha-amylase and glucoamylase activities in the pancreas, SI length and SI digesta weight. Forage-fed calves gained faster (P less than .01) and had greater (P less than .05) pancreatic protein concentrations, alpha-amylase and glucoamylase activities in the pancreas and greater SI digesta alpha-amylase activities than grain-fed calves did. Increased feed intake increased (P less than .01) mucosal weight/cm small intestine only in forage-fed calves and increased (P less than .05) SI surface/volume only in grain-fed calves. Mucosal weight was greatest (P less than .05) at the terminal ileum, surface/volume was greatest (P less than .05) in the duodenum, and mucosal protein concentration was highest (P less than .05) in the SI mid-section. Mucosal lactase was higher (P less than .05) in proximal segments, whereas mucosal isomaltase was higher in middle and distal segments of the small intestine. For mucosal maltase activity, there was a feed intake x SI sampling site interaction (P less than .05) and for trehalase, a diet x feed intake x SI sampling site interaction (P less than .05). The SI distribution patterns of maltase and isomaltase were similar, as were those of trehalase and lactase. The alpha-amylase activity in the pancreas and SI morphology were influenced greatly by diet composition and feed intake by calves.     

Influence of dietary zinc and copper on digestive enzyme activity and intestinal morphology in weaned pigs

The current study was conducted to investigate the effects of high dietary concentrations of Zn as zinc oxide and Cu as copper sulfate on the activity of digestive enzymes in the pancreas and the intestinal mucosa, intestinal morphology, and mucin histochemistry in pigs after weaning. Thirty-two pigs were weaned at 4 wk of age. The pigs were fed standard weaning diets supplemented with Zn (100 or 2,500 ppm) and Cu (0 or 175 ppm) in a 2 x 2 factorial arrangement of treatments for a 14-d period. In pancreatic tissue, the activity of amylase, carboxypeptidase A, chymotrypsin, trypsin, and lipase increased (P < 0.01) in pigs fed 2,500 ppm of Zn, whereas the activity of carboxypeptidase B and carboxylester hydrolase was unaffected. Copper had no effect on the activity of pancreatic enzymes. In small intestinal contents, the total activity of amylase and carboxypeptidase A was greater in pigs fed 100 ppm of Zn (P < 0.05), whereas feeding 2,500 ppm of Zn increased the chymotrypsin activity (P < 0.001). The remaining enzymes were unaffected by dietary Zn concentration. The villi were longer in the cranial small intestine (P < 0.001) in pigs fed 100 ppm of Zn than in pigs fed 2,500 ppm of Zn, but otherwise there were no clear effects of Zn and Cu supplementation on intestinal morphology. In the cranial small intestine, the activity of maltase (P < 0.001), sucrase (P < 0.001), and lactase was greater in pigs fed 100 ppm of Zn, even though there was a Zn x Cu interaction (P < 0.05) in lactase activity. In the middle and caudal small intestine, no clear differences between dietary treatments were observed. The activity of gamma-glutamyl transpeptidase in the intestinal mucosa was not affected by dietary Zn or Cu. In pigs fed 100 ppm of Zn, the activity of aminopeptidase N was greater in the caudal small intestine, but dietary Zn or Cu had no effect on aminopeptidase N in the cranial and middle small intestine. No effect of dietary Zn or Cu supplementation was found on carbohydrate histochemistry in the caudal small intestine, whereas high dietary Zn increased the area of neutral, acidic, and sulfomucins in the cecum (P < 0.01) and in the colon (P < 0.001). In summary, high dietary Zn increased the activity of several enzymes in the pancreatic tissue and increased the mucin staining area in the large intestine, whereas Cu had no clear effect on these variables. However, no definite answers were found as to how the growth promoting and diarrhea reducing effects of excess dietary Zn are exerted.     

Influence of alpha-linked glucose on sodium-glucose cotransport activity along the small intestine in cattle

Thirteen steers (378+/-23 kg) were used in a split-plot experimental design to evaluate the effect of small intestinal carbohydrate on sodium-glucose cotransport in brush border membrane vesicles prepared from five equidistant sites along the small intestine. The steers consumed 7.2+/-0.4 kg/d ground fescue hay and soybean meal-based supplement and were infused ruminally or postruminally with a partial alpha-amylase starch hydrolysate (914.5+/-8.3 g/d) for 7 d. On d 7, five equidistant 1-m small intestinal sections were harvested and frozen in liquid N for later preparation of brush-border membrane vesicles. Maltase activity of the homogenate and vesicle preparations changed (P < 0.001; lowest in the duodenum, highest in the jejunum) and alkaline phosphatase decreased (P < 0.001) along the small intestine. With respect to the original homogenates, the vesicle preparations were enriched 9.80+/-0.83- and 7.64+/-0.67-fold for alkaline phosphatase and maltase, respectively; enrichments were not different between treatments (P = 0.76 and 0.39, respectively). However, alkaline phosphatase and maltase enrichment changed (P < 0.001) along the small intestine. Recoveries of alkaline phosphatase and maltase activities (25.0+/-0.2% and 19.5+/-0.2%, respectively) in the vesicle preparation were not affected (P = 0.29 and 0.21, respectively) by treatment but changed (P < 0.001) along the intestine. Recovery of protein in the vesicle preparation was 2.60+/-0.01% and was not affected by treatment or intestinal site. Sodium-glucose cotransport activity (220+/-44 pmol x mg(-1) x s(-1)) was not affected (P = 0.34) by treatment but did change (P < 0.001; lowest in the ileum, highest in the proximal and mid-jejunum) along the small intestine. Apparent Km of the sodium-glucose cotransporter for glucose was 62.8+/-5.8 microM. The specific activity of maltase was highest in the jejunum, and sodium-glucose cotransport was highest in the first two jejunal sites. However, duodenal maltase activity was lowest and ileal sodium-glucose cotransport activity was lowest. Sodium-glucose cotransport activity may limit small intestinal starch assimilation in the distal small intestine. It does not seem that glucose arising from carbohydrate hydrolysis regulates activity of sodium-dependent glucose transport in cattle.     

Stimulation by colostrum or mature milk of gastrointestinal tissue development in newborn pigs

Porcine colostrum and milk were orally administered to newborn pigs to evaluate their gastrointestinal growth-promoting activity. Five piglets per treatment group were gavage-fed 5% lactose (L), defatted colostrum (C) or defatted mature milk (d 16 of lactation) (M) at 3-h intervals over a 24-h period. Colostrum and milk were administered on equivalent dry matter basis and all piglets received 1 mCi of [3H]thymidine per kg BW at the onset of feeding. Small intestines of C- and M-fed pigs were 1.6-and 1.3-fold, respectively, the weight of small intestines of those fed L (P less than .01). Total DNA content of intact small intestines were not different among groups; however, cpm [3H]thymidine/mg intestinal DNA of C and M piglets exceeded (P less than .05) that for L piglets. DNA content and cpm [3H]thymidine of intestinal mucosa did not differ among groups. Total protein in the intestines and intestinal mucosa of C pigs exceeded (P less than .01) that for L and M pigs. Total RNA in the small intestine and intestinal mucosa were similar for C and M groups but less (P less than .01) for L piglets. Stomach and pancreas weights among all pigs were similar, although C and M pigs exceeded L pigs in stomach (P less than .01) and pancreas (P less than .01) RNA content. In contrast, no differences in stomach DNA, protein and cpm [3H]thymidine or in pancreatic DNA, protein and cpm [3H]thymidine were detected. SDS-polyacrylamide gel electrophoresis was used to identify qualitative and quantitative differences in the protein compositions of porcine colostrum and mature milk.(ABSTRACT TRUNCATED AT 250 WORDS)     

The possible effects of gastro-intestinal nematodes upon intestinal enzymes of calves

Observations were made on the effect of combined infections of gastro-intestinal nematodes on small intestinal disaccharidases and alkaline and acid phosphatases in 4–5-month old Friesian calves. The tests were carried out 3 weeks following exposure of these calves to infected pasture in a wet tropical environment.Sucrase activity, at a very low level, was detected in all parts of the small intestine of infected and uninfected calves. There was no significant difference in maltase, trehalase, cellobiase, sucrase, lactase, acid β-galactosidase, acid and alkaline phosphatase activities between uninfected control calves and all infected calves in which Cooperia species predominated. In heavily infected calves with worm burdens greater than 20 000 Cooperia species significantly elevated (P < 0.05) duodenal maltase and acid phosphatase levels were recorded.     

Impact of Yersinia enterocolitica enteritis on disaccharidase activity and small intestinal morphology in colostrum-deprived newborn piglets

The effect of enteritis on the development of the small intestine was examined in newborn, colostrum-deprived piglets infected with a human isolate of Y. enterocolitica (serotype 0:3, biotype 4) soon after birth. The piglets were killed 3 days (n = 6) or 5 days (n = 8) after infection, or antibiotic therapy was commenced on day 5 and the animals killed on day 14 (n = 5). Compared with the non-infected controls, infected animals had reduced mucosal lactase and sucrase, but not maltase activity, while after antibiotic therapy, previously infected piglets had a lower lactase and a higher maltase and sucrase activity. Lactase activity was significantly reduced in the duodenum and jejunum, and mean values were lower in the ileum, but the difference did not reach significance; maltase activity was greater at all ages from the distal jejunum to the mid-ileum; sucrase activity was reduced in all segments up to day 5 but after antibiotic therapy was increased in the jejunum and appeared early in the ileum. Enzyme profiles were more mature along the crypt-villus axis in some segments of the intestine in previously infected piglets. Sodium-potassium-ATPase activity was unchanged. There was a reduced villus height:crypt depth ratio, crypt hyperplasia and increased crypt cell proliferation. Morphological maturation, indicated by loss of vacuoles and location of the nucleus at the base of the enterocyte, proceeded distally from the duodenum to ileum from 3 to 14 days of age when only the ileum remained immature. In infected piglets, there was reduced vacuolation and earlier location of the nucleus at the base of the cell in the distal intestine. Accelerated maturity of specific disaccharidases and enterocyte morphology in infected piglets appears to be due to physical damage to the mucosa resulting in faster proliferation of crypt cells and migration of enterocytes. It is suggested that this may reduce macromolecular internalisation and impair the ability to utilise dietary carbohydrate and may have long-term effects on growth and immunological responses of the gut.